1.

Rhinosinusitis akut, kronik

2. jenis2 ISPA dan komplikasinya
3. Kelainan telinga luar dan tengah apa saja dan penyebabnya apa saja
4. Gangguan pendengaran secara umum (tuli kondukfit dan sensorineural)

CO/WO Jumat (13/9/2019)

1. Anatomi telinga ringkas
a. struktur2 yang membentuk, kondusi normalnya spt apa
b. dari telinga luar, tengah, dalam
c. batas2 telinga luar, tengah, dalam
d. kelainan/penyakit yg bs terjadi di situ
i. tau! Fungsi tuba eustachius dan apa gangguan tuba

2. Fisiologi pendengaran
e. hantaran getaran
f. struktur yg terlibat
g. 3 jenis tuli —> lokasinya dan masing2 cari contoh etiologinya

3. Tipe2 rhinitis
h. cari gejala dan tanda singkat aja masing2
i. khusus buat rhinitis alergi, cari trias alergi, diagnosis menurut WHO ARIA 2001 dan klasifikasi WHO ARIA 2001
+ tx

4. Rhinitis akut
j. definisi
k. anam + pf
l. ddx
m. treatment
n. komplikasi —> dia bisa bikin apa ke struktur THT lainnya

5. OME
o. definisi
p. sign + symptoms
q. faktor resiko
r. terjadi karena apa
s. ddx: baca OMA (definis + stadium aja), OMSK (definisi + stadium)

6. Pemeriksaan garpu tala + intepretasi —> udah pernah di LO in

7. Audiometri —> cara baca dan intepretasi —> udah pernah di LO in

8. PF THT nanti aku tanya2 ya
t. baca ttg manuver valsava dan tony bee





EAR PAIN



HEARING LOSS



Conductive hearing loss

Otoscopy – abnormal outer ear:

• ï Impacted cerumen: with ear fullness; obvious on otoscopy. If severe, consider keratosis obturans. Clean and re-examine
for other dx! Hearing loss from this cause never exceeds 40dB.
• ï Otitis externa: with otalgia, discharge, puritus, and erythema. Ddx bacterial infection from otomycosis (fungal spores).
Treat and re-examine: beware the otitis externa 2° to otitis media + TM perforation. Note: pain may be referred to the ear
from sites supplied by CN IX-X (e.g. pharynx, larynx).
• ï Tumor: SCC, BCC. Usually misdiagnosed as otitis externa and only suspected after treatment failure.
• ï Foreign body


Otoscopy – abnormal tympanic membrane (TM):

• ï Otitis media: ear fullness & pain (accumulated pus pressing on the TM), hearing loss (fluid preventing TM vibration), ±
pyrexia or systemic upset. The TM appears bulging, red, and inflammed.
• ï Otitis media with effusion (glue ear, secretory otitis media): due to poor middle ear ventilation or eustachian tube
dysfunction. TM appears grey & dull ± prominent blood vessels ± bubbles. Always look for a cause – e.g. nasopharyngeal
CA (esp if unilateral glue ear), swollen adenoids.
• ï Chronic suppurative otitis media: a non-healing TM perforation, visible on otoscopy, causing mild hearing loss &
otorrhoea (if active; dry if inactive).
• ï Cholesteatoma: a growth of desquamated epithe- lium which invariably becomes infected, causing conductive hearing loss
& foul-smelling discharge. A chronically draining ear that fails to respond to antibiotics should prompt suspicion. Exam
shows infected discharge, TM with attic retraction or TM perforation. Left alone, the cholesteatoma may erode adjacent
structures, causing sensorineural hearing loss, facial palsy, vertigo, intracranial sepsis, and sagittal sinus thrombosis.
• ï TM rupture: 2° foreign body, barotrauma, or head injury - usually apparent from hx.

Normal otoscopy:

• ï Otosclerosis: bony overgrowth causing fixation of stapes. Hearing loss is usually bilateral, presenting btw late teens – 40
yrs old, and progressive; there may also be a component of sensorineural hearing loss. Surgical exploration confirms the dx.
Sensorineural hearing loss

Unilateral – sudden-onset:

• Vestibular neuritis: sudden-onset hearing loss and bad vertigo, often after viral URTI. See approach to giddiness – dizziness
recovers but hearing may not.

• Idiopathic sudden sensorineural hearing loss: acute onset hearing loss ± tinnitus, or blocked ear. By defintion, otoscopy
and MRI must be normal (MRI excludes a stroke and haemorrhage into an acoustic neuroma). Exclude hyperthyroidism and
syphillis which are reversible causes, as well as DM and hepatitis if high-dose steroids are considered.

• Cerebrovascular: sudden-onset sensorineural loss, vertigo ± other CN deficits – due to stroke or TIA affecting inner ear or
brainstem

• Neurological: e.g. multiple sclerosis.

Unilateral – episodic or chronic:

• Meniere dx: episodic aural fullness, hearing loss or tinnitus, severe vertigo with nystagmus, nausea/ vomiting, lasting up to
4h. Sensorineural hearing loss is initially unilateral, low-frequency, and present only during attacks, but may progress to
become permanent or bilateral.

• Acoustic neuroma (cerebellopontine angle tumor): usually expands slowly but haemorrhage into the tumor can cause
sudden symptoms including CN VII deficit (rare otherwise).

• Post-infective: residual hearing impairment after meningitis (esp children) or labyrinthitis

Bilateral:

• Presbycusis: a progressive degenerative disease of the elderly, presenting as symmetrical sensorineural hearing loss most
affecting higher frequencies. Loss of hair cell receptors causes difficulty hearing in a noisy environment.

• Noise exposure: elicit occupational or recreational exposure to loud noise.

• Drug ototoxicity: fr aminoglycosides, frusemide, chemo (cisplatin, 5-FU), erythromycin, tetracycline, etc. Take a full drug hx
and elicit risk factors e.g. poor renal function.

• Systemic: anemia, hypo/hyperthyroid, autoimmune

Either type of hearing loss:

• ï Mixed hearing loss: due to pathology of both middle and inner ear, e.g. cholesteatoma with local invasion, otosclerosis
involving ossicles & cochlea, chronic otitis media, tumors.
• ï Trauma: causes sensorineural hearing loss due to temporal bone fracture, or conductive hearing loss due to ossicular chain
disruption
• ï Congenital: conductive loss e.g. outer ear atresia, ossicular chain malformation or sensorineural loss e.g. inherited,
intrauterine infection. This may be apparent from birth or progressive with age, syndromic or non-syndromic; ask for family
hx

Tinnitus with no hearing loss 
Listen for objective tinnitus (can be heard by both pt and dr), which may be pulsatile, clicking, or due
to an insect 


• Pulsatile tinnitus: tinnitus sounding like ‘gushes’ (of blood) or like a ‘hearbeat’ often has good reason to sound such. The
etiology is commonly vascular – paraganglioma (e.g. glomus jugulare), dural arterio- venous fistula, or arterial bruit from
stenosis. This should prompt investigation (MR or angiography)

• Clicking tinnitus: often palatal myoclonus due to underlying brainstem dx or multiple sclerosis, spasm of middle ear
muscles, or temporo- mandibular joint dysfunction.

• Respiration sounds: eustachian tube dysfunction.

• Buzzing sounds: consider an insect in the external ear

• Auditory hallucinations: in temporal lobe epilepsy or psychiatric dx (e.g. schizophrenia, depression – may be voices or just
sounds).

SORE THROAT



ACUTE RHINITIS
• Tipe nya bisa viral, bacterial, atau iritative

VIRAL RHINITIS
• Common cold(coryza)
§ Etiologi:
• grgr virus. Biasanya nyebar lewat droplets.
• Virusnya: adenovirus, picornavirus and its subgroups such as rhi- novirus, coxsackie virus and enteric
cytopathic human orphan virus
• Inkubasinya: 1-4 hari dan illness nya biasanya 2-3 weeks.
§ Clinical features:
• Burning sensation di back of nose
• Diikuti nasal stuffiness, rhinorrhea, sneezing
• Chilly and low-grade fever
• Nasal discharge nya watery and profuse, kaddang bisa mucopurulent grgr ada seconadry infection oleh
bakteri
o Streptococcus haemolyticus, pneumococcus, Staphylococcus, Haemophilus influenzae, Klebsiella
pneumoniae and Moraxella catarrhalis.
§ Treatment
• Bed rest
• Plenty fluids
• Antihistamine
• Nasal decongestant
• Analgesic buat kalo ada headache, fever, myalgia
o Kalo bisa analgesic nya ga ada aspirin karena aspirin bikin shedding virus naik
• Antibiotik butuh kalo ada infeksi secondary
§ Complications
• Self limiting biasanya 2-3 minggu
• Komplikasi: sinusitis, pharyngitis, tonsillitis, bronchitis, pneumonia and otitis media may result
INFLUENZA RHINITIS
• Influenza viruses A, B or C are responsible.
• Symptoms and signs are similar to those of common cold.
• Complications due to bacterial invasion are common.

RHINITIS ASSOCIATED WITH EXANTHEMAS
• Measles, rubella and chickenpox are often associated with rhinitis which precedes exanthemas by 2–3 days.
• Secondary infection and complications are more frequent and severe.

BACTERIAL RHINITIS
• Nonspecific infections
o Bisa primary and secondary
§ Primary:
• di anak kecil n biasa grgr infeksi pneumococcus, streptococcus or staphylococcus
• greyish white tenacious membrane bisa aad ddi iidung, kalo mau coba remove bisa bikin
bleeding
§ secondary
• result dari infeksi bakteri viral
• Diphteritic rhinitis
o Jarang ada
o Bisa primary bisa secondary
o A greyish membrane covering si inferior turbinate and the floor of nose; membrane is tenacious(nempel) and
its removal causes bleeding.
o Excoriation of anterior nares and upper lip may be seen.
o Treatment: isolasi bakteri, systemic penicillin + diphteria antitoxin

IRRITATIVE RHINITIS
• caused by exposure to dust, smoke or irritating gases such as ammonia, formaline, acid fumes, etc.
• result from trauma inflicted on the nasal mucosa during intranasal manipulation, e.g. removal of a foreign body.
• Clinical features: sudden sneezing, rhinorrhoea and nasal congestion.
• Treatment: remove dust atau agent nya itu

CHRONIC RHINITIS

Chronic nonspecific inflammations of nose include:
1. Chronic simple rhinitis.
2. Hypertrophic rhinitis.
3. Atrophic rhinitis.
4. Rhinitis sicca.
5. Rhinitis caseosa.

1. Chronic simple rhinitis
a. Etiologi
i. Recurrent attack dari acute rhinitis
1. Persistence of nasal infection due to sinusitis, tonsillitis and adenoids.
2. Chronic irritation from dust, smoke, cigarette smoking, snuff, etc.
3. Nasal obstruction due to deviated nasal septum, synechia leading to persistence of discharge
in the nose.
4. Vasomotor rhinitis
5. Endocrinal or metabolic factors -> hypothyroid, kebanyakan carbohydrate, lack of exercise
b. Pathology
i. Simple chronic rhinitis itu early stage dari hypertrophic rhinitis
ii. Tampak ada hyperemis + edema mucous membrane dengan hypertrophy dari seromucinous glands
iii. Ada increase dari goblet cells
iv. Bisa ada blood kalo ada turbinates yang distended
c. Clinical features
i. Nasal obstruction: tambah parah kalo lying dan affect satu sisi hidung
ii. Nasal discharge: bisa mucoid atau mucopurulent, thick, dan viscid. Bisa ada post nasal drip. Pasien
pengen blow the nose atau clear the throat terus
iii. Headache: grgr swollen turbinates ngejepit si nasal septum
iv. Swollen turbinates: nasal mucosa nya warna dull red. Turbinate nya swollen. Middle turbinate jg bisa
swollen dan ngejepit si septum.
1. they pit on pressure
v. Postnasal discharge: mucoid atau mucopurulent discharge keliatan di posterior pharyngeal wall
d. Treatment
i. Kurangin smoking or alcohol, environment or work situation (smoky or dusty surroundings).
ii. Nasal irrigations pake alkaline solution : ngebuang viscid secretions and also remove superficial
infection.
iii. Nasal decongestants : relieve nasal obstruction and improve sinus ventilation. Excessive use of nasal
drops and sprays should be avoided because it may lead to rhinitis medicamentosa. A short course of
systemic steroids helps to wean the patients already addicted to excessive use of decongestant drops
or sprays.
iv. Antibiotics help to clear nasal infection and concomitant sinusitis.
2. Hypertrophic rhinitis
a. Characterized by: thickening of mucosa, submucosa, seromucinous glands, periosteum and bone. Keliatan ada
changes di turbinates
b. Etiologi
i. Recurrent nasal infections, chronic sinusitis, chronic irritation of nasal mucosa grgr smoking, industrial
irritants, prolonged use of nasal drops and vasomotor, and allergic rhinitis
c. Symptoms:
i. Nasal obstruction -> symptoms utama
ii. Nasal discharge nya thick and sticky
iii. Headache, heavy head
iv. Transient anosmia
d. Signs
i. hypertrophy of turbinates
ii. Turbinal mucosa is thick and does not pit on pressure.
iii. It shows little shrinkage with vasoconstrictor drugs due to presence of underlying fibrosis.
iv. Mullberry appearance
e. Treatment
i. Reduction size:
1. Linear cauterization.
2. Submucosal diathermy.
3. Cryosurgery of turbinates.
 4. Partial or total turbinectomy. Hypertrophied inferior turbinate can be partially removed at its
anterior end, inferior border or posterior end. Middle turbinate, if hypertrophied, can also be
removed partially or totally. Excessive removal of turbinates should be avoided as it leads to
persistent crusting.
5. Submucous resection of turbinate bone. This removes bony obstruction but preserves
turbinal mucosa for its function.
6. Lasers have also been used to reduce the size of turbinates.
3. ATROPHIC RHINITIS (OZAENA)
a. chronic inflammation of nose characterized by atrophy of nasal mucosa and turbinate bones
b. The nasal cavities are roomy and full of foul-smelling crusts.
c. 2 tipe: primary and secondary
i. primary atrophic rhinitis
1. etiology
a. hereditary factors
b. endocrinal disturbance -> starts pas puberty, lebih sering di cewe. Ilang biasanya pas
menopause
c. racial factors -> White and yellow
d. nutritional deficiency-> vit a,d, iron
e. infective -> Various organisms have been cultured from cases of atrophic rhinitis
such as Klebsiella ozaenae, (Perez bacillus), diphtheroids, Proteus vulgaris,
Escherichia coli, staphylococci and streptococci
f. autoimmune process -> The body reacts by a destructive process to the antigens
released from the nasal mucosa. Viral infection or some other unspecified agents
may trigger antigenicity of nasal mucosa
2. pathology
a. Ciliated columnar epithelium is lost and is replaced by stratified squamous type.
There is atrophy of seromucinous glands, venous blood sinusoids and nerve
elements. Arter- ies in the mucosa, periosteum and bone show obliterative
endarteritis. The bone of turbinates undergoes resorption causing widening of nasal
chambers. Paranasal sinuses are small due to their arrested development.
3. Clinical features
a. Foul smell from nose. Tp dia ga nyadar grgr dia anosmia
b. Nasal obstruction, walapum wide nasal chambers-> ini ggr large crust fill the nose
c. Kalo diremove bisa epistaxis
d. full of greenish or greyish black dry crusts covering the turbinates and septum.
e. When the crusts have been removed, nasal cavities appear roomy with atrophy of
turbinates so much so that the posterior wall of nasopharynx can be easily seen.
f. Nasal mucosa appears pale.
ii. Secondary atrophic rhinitis
1. Specific infections like syphilis, lupus, leprosy and rhinoscle- roma may cause destruction of
the nasal structures leading to atrophic changes.
4. RHINITIS SICCA
a. It is also a crust-forming disease seen in patients who work in hot, dry and dusty surroundings, e.g. bakers,
iron- and gold- smiths. Condition is confined to the anterior third of nose particularly of the nasal septum.
Here, the ciliated columnar epithelium undergoes squamous metaplasia with atrophy of seromucinous glands.
Crusts form on the anterior part of septum and their removal causes ulceration and epistaxis, and may lead to
septal perforation.
b. Treatment consists of correction of the occupational sur- roundings and application of bland ointment or one
with an antibiotic and steroid to the affected part. Nose pricking and forcible removal of crusts should be
avoided. Nasal douche, like the one used in cases of atrophic rhinitis, is useful.
5. RHINITIS CASEOSA
a. It is an uncommon condition, usually unilateral and mostly affecting males.
b. Nose is filled with offensive purulent discharge and cheesy material. The disease possibly arises from chronic
sinusitis with collection of inspissated cheesy material. Sinus mucosa becomes granulomatous. Bony walls of
sinus may be destroyed, requiring differentiation from malignancy. Treat- ment is removal of debris and
granulation tissue and free drainage of the affected sinus. Prognosis is good.

ALLERGIC RHINITIS
• IgE-mediated immunologic response of nasal mucosa to airborne allergens and is characterized by watery nasal
discharge, nasal obstruction, sneezing and itching in the nose. This may also be associated with symptoms of itch- ing in
the eyes, palate and pharynx. Two clinical types have been recognized:
o Seasonal. Symptoms appear in or around a particular season when the pollens of a particular plant, to which
the patient is sensitive, are present in the air.
 o Perennial. Symptoms are present throughout the year.
• Etiologi
o Inhalant allergens
§ Bisa seasonal bisa prennial
§ pollens from trees, grasses and weeds.
§ molds, dust mites, cockroaches and dander from animals.
• Dust includes dust mite, insect parts, fibres and animal dan- ders.
• Dust mites live on skin scales and other debris and are found in the beddings, mattresses,
pillows, carpets and upholstery.
o Genetic predisposition
§ Kalo salah satu allergi, anaknya 20% allergy. Kalo ddua dduanya alergi 47% anaknya alergi

•
• Pathogenesis
o Inhaled allergen bakal produce specific ige antibody di badan
o Ige antibody ini bakal nempel sama blood basophils atau mast cell
o Ini bakal bikin degranulasi mast cell dan release chemical mediatros

o
o dia bisa ada vasodilatasi, edema mucosa, infiltrasi eosinopil, excessive secretion dari nasal glands dll
o allergic response occurs in 2 phases
§ acute or early phase
• 5-30 menit awal stelah exposure allelrgen
 • lgsg sneeze, rhinorhea nasal blockage, or bronchospasm
• ini grgr release si histamine
§ late or delayed phase
• 2-8 jem stelah exposure allergen
• ini grgr infiltrasi inflamatory cells- eosinopil, neutrophil, basophil, monocytes dadn cd4 dan t
cells di site nya yg bikin swell, congestion, dadn thick scretion
• clinical features
o nasal signs
§ ya gitu ada watery discharge, swollen turbinates, pale andd ededma nasam mucosa bluish jg
o Ocular signs
§ oedema of lids, congestion and cobblestone appearance of the conjunctiva, and dark circles under the
eyes (allergic shiners).
o Otologic signs
§ retracted tympanic membrane or serous otitis media as a result of eustachian tube blockage.
o Pharyngeal signs
§ granular pharyngitis due to hyperplasia of submucosal lymphoid tissue. A child with perennial allergic
rhinitis may show all the features of prolonged mouth breathing as seen in adenoid hyperplasia.
o Laryngeal signs
§ hoarseness and oedema of the vocal cords.
• Diagnosis
o Test bloodd and diff count
o Nasal smear bakal kloiatan banyak eosinophil
o Skin test prick dan specific ige measurement
o Radioallergosorbent test (RAST).
§ It is an in vitro test and measures specific IgE antibody concentration in the patient’s serum.
o Nasal provocatio ntest
§ A crude method is to challenge the nasal mucosa with a small amount of allergen placed at the end of
a toothpick and asking the patient to sniff into each nostril and to observe if allergic symptoms are
repro- duced.
• complications
o Recurrent sinusitis because of obstruction to the sinus ostia.
o Formation of nasal polypi in about 2%.
o Serous otitis media.
o Orthodontic problems and other ill-effects of prolongedmouth breathing especially in children.
o Bronchial asthma
• Treatment
o Avoidance of allergen.
o Treatment with drugs.
§ Antihistamine
§ Sympathomimetic ddrugs
• Alpha-adrenergic drugs constrict blood vessels and reduce nasal conges- tion and oedema.
• Pseu- doephedrine and phenylephrine are often combined with antihistaminics for oral
administration.
• Topical use of sympathomimetic drugs causes nasal decongestion. Phenylephrine,
oxymetazoline and xylo- metazoline are often used to relieve nasal obstruction, but are
notorious to cause severe rebound congestion.
§ Corticosteroid
• Topical steroids such as beclomethasone dipropio- nate, budesonide, flunisolide acetate,
fluticasone and mometasone inhibit recruitment of inflammatory cells into the nasal mucosa
and suppress late-phase allergic reaction,
§ Sodium cromoglycate.
• It stabilizes the mast cells and pre- vents them from degranulation despite the formation of
IgE-antigen complex.
§ Anticholinergics.
• They block rhinorrhoea both of the allergic and nonallergic rhinitis. Ipratropium bromide has
been used as nasal spray to control rhinorrhoea.
§ Leukotriene receptor antagonists.
• They include montelu- kast, pranlukast and zafirlukast. They block cysteinyl leukotriene type
receptors. They are well-tolerated and have few side effects.
§ Anti-IgE.
• It reduces the IgE level and has an anti- inflammatory effect. Omalizumab is such a drug->
gadipakeeee
o Immunotherapy.
§ Immunotherapy or hyposensitization is used when drug treatment fails to control symptoms or
produces intolerable side effects. Allergen is given in gradu- ally increasing doses till the maintenance
dose is reached. Immunotherapy suppresses the formation of IgE. It also raises the titre of specific IgG
antibody. Immunotherapy has to be given for a year or so before significant improvement of
symptoms can be noticed. It is discontinued if uninter- rupted treatment for 3 years shows no clinical
improvement.
ACUTE SINUSITIS

• Etiologi
o Exciting causes
§ Nasal infections.
• Most common cause of acute sinusitis is viral rhinitis followed by bacterial invasion.
§ Swimming and diving.
• Infected water can enter the sinuses
§ Trauma.
• Compound fractures or penetrating injuries of sinuses—frontal, maxillary and ethmoid—may
permit direct infection of sinus mucosa.
§ Dental infections.
• Maxillary sinus.
• Infection from the molar or premolar teeth or their extraction may be followed by acute
sinusitis.
o Predisposing causes
§ Local
• Obstruksi sinus ventilation and drainage -> normal nya ada cilia bantu drainage. Kalo ada
masalah:
o Nasal packing
o Deviated septum
o Hypertrophic turbinates
o Oedema of sinus ostia due to allergy or vasomotor rhinitis
o Nasal polypi
o Structural abnormality of ethmoidal air cells
o Benign or malignant neoplasm.
• Stasis of secretions in the nasal cavity
o Secretion gabisa darinage ke nasopharynx krn viscocity nya tinggi misal cystic
fibrosis
o Bisa juga grgr obstruction (enlarged adenois, choanal atresia) trus infeksi de
• Previous sinusitis
o Local defences of sinus mucosa are already damaged.
§ General
• Environment
o Cold wet climate
o Polusi, smoke, dust, overcrowed
• Poor health
o Exanthema fever measle chicken pox whooping cough
o Nutrition dedf
o Systemic dzz suchas dm, immune def syndrome
§ Bacteriology
• Awalnya cuma viral biasanya tp diikuti bacterial invasion
• Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Streptococcus
pyogenes, Staphylococcus aureus and Klebsiella pneu- moniae.
o Pathology
Sinusitis per tempat…. Print aja de
Trus chronic sinusitis.. print jg aja deh capek
Truss complication nyaaa.. intinya dia bisa kmana mana dan salah satunya bikin otitis media yay!

HEARING LOSS