TUGAS THT Nurul Jadi

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    TUGAS THT

    Diajukan untuk Memenuhi Tugas dan Melengkapi Syarat dalam Menempuh Program Pendidikan

    Profesi Dokter di Bagian Ilmu Kesehatan THT-KL

    S!D Tugurejo Semarang

    Disusun oleh "

    #urul $fifah

    %&'(%)'*+,(

    $K!LT$S K.D/KT.$#

    !#I0.SIT$S ISL$M S!LT$# $1!#1

    S.M$$#1

    (%&2

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    &' Kriteria diagnosis sinusitis 3erdasarkan task for4e5 saphiro dan ra4helesky

    $' Sinusitis akut menurut Task or4e

    M$6/ MI#/

    - #yeri pada 7ajah

    - /3struksi nasal 8 hidung 3untu

    - Post nasal drip

    - Hiposmia 8anosmia

    - Se4ret nasal purulen

    - Demam 9 akut:

    - Kongesti nasal

    - #yeri gigi 9 terutama gigi

    geraham:

    - Sakit kepala

    - Halotosis

    - Batuk

    - Demam 9kronis:

    - asa lelah- Sakit telinga 8 terasa ada

    tekanan di telinga 8 perasaan

    penuh di telinga

    ; Di4urigai 3ila didapatkan ( gejala mayor atau & gejala mayor dan ( gejala minor atau

    le3ih dengan gejala < + hari=

    B' Sinusitis kronis menurut Saphiro Dan a4helesky

    Mayor Minor

    1ejala dan tanda - Se4ret hidung yang

    purulen

    - Se4ret faring yang

    purulen

    - Batuk

    - .dem praor3ita

    - #yeri pada 7ajah

    - #yeri pada gigi

    - Disfagia

    - Mengi

    - #yeri kepala

    - /talgia

    - Halitosis

    - Demam 9 kronis:Diagnosis - gam3aran radiologi

    7ater>s terdapat

    - pemeriksaan sitologi

    nasal neutrofil atau

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    osifikasi5 air fluid

    le?el atau

    pene3alan mukosa

    *%@ dari antrum

    - sintigrafi karena

    terdapat pene3alam

    8 opafikasi sinus

    3akteremia

    - pemeriksaan

    ultrasonografi

    Diagnosis klinis "

    - 1ejala dan tanda ( kriteria mayor atau & mayor dan ( minor

    - Pemeriksaan diagnosti4 " & mayor " konfirmasi

    & minor " menyokong

    ; diagnosis ditegakkan 3ila gejala terse3ut le3ih dari 2 3ulandengan atau tanpa

    mem3utuhkan anti3ioti4 ;

    2. Harga normal diffcount

    #ilai #ormal La3oratorium Patologi Klinik

    PRIA

    HematologiAenis Spesimen " darah

    Darah Lengkap

    .ritrosit " ,'* *'C 9,'* *'*: 9juta8ul:

    Haemoglo3in 9H3: " &2'* &+'* 9&2 &: 9g8dl:Hematokrit 9Ht: " ,&'% *2'% 9,% *,: 9@:

    http://panji1102.blogspot.com/2008/10/nilai-normal-laboratorium-patologi.htmlhttp://panji1102.blogspot.com/2008/10/nilai-normal-laboratorium-patologi.html
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    Trom3osit " &*%'%%% ,,%'%%% 9&*%'%%% ,%%'%%%: 98ul:

    Leukosit " ,'%%% &&'%%% 9*'%%% &%'%%%: 98ul:

    Laju .ndap Darah 9L.D: " % &% 9mm8jam:

    Diff count / Hitung Jenis eu!osit

    Basofil " % & 9@:

    .osinofil " & 2 9@:

    Batang " ( 9@:

    Segmen " *% +% 9@:

    Limfosit " (% ,% 9@:

    Monosit " ( ) 9@:

    Urinalisa

    Aenis Spesimen " urine midstream 8 porsi tengah

    !rine Lengkap

    Earna " kuning

    Kejernihan " jernih

    1lukosa " negatifBiliru3in " negatif

    Keton " negatif

    Berat jenis " &'%%* &'%2% 9&'%%2 &'%2%:

    Darah samar " negatif

    pH " ,'* )'% 9* ):

    Protein " negatif

    !ro3ilinogen " %'& &'% 9.!8dl:

    #itrit " negatif

    .sterase leukosit " negatif

    Sedimen

    Leukosit " % * 9% 2: 98LPB:

    .ritrosit " % & 98LPB:

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    Silinder " negatif 98LPK:

    .pitel " F&

    Kristal " negatif

    Lain-lain " negatif

    "imia Dara#

    1lukosa # " )% &%% 9mg8dl:

    1lukosa PP " &%% - &(% 9mg8dl:

    1lukosa S " G &*% 9mg8dl:

    Kolesterol total " G (%% 9mg8dl:

    Trigliserida " G &*% 9mg8dl:

    HDL Kolesterol " < ** 9mg8dl:

    LDL kolesterol " G &*% 9mg8dl:

    !reum " &* ,% 9mg8dl:

    Kreatinin " %'* &'* 9mg8dl:

    $sam urat " 2', +'% 9mg8dl:

    Biliru3in total " %'( & 9mg @:

    Biliru3in direk " % %'( 9mg @:

    Biliru3in indirek " %'( %') 9mg @:

    S1/T " * ,% 9u8l:

    S1PT " * ,& 9u8l:

    $lkali osfatase " ,* &C% 9iu8l:

    1amma 1T " () 9mu8ml:

    Protein total " '& )'( 9gr @:

    $l3umin " 2') *'% 9gr @:

    1lo3ulin " ('2 2'( 9gr @:

    $A%ITA

    Hematologi

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    Aenis Spesimen " darah

    Darah Lengkap

    .ritrosit " , * 9juta8ul:

    Haemoglo3in 9H3: " &( &* 9g8dl:

    Hematokrit 9Ht: " 2 ,+ 9@:

    Trom3o sit " &*%'%%% ,%%'%%%98ul:

    Leukosit " *'%%% &%'%%%98ul:

    Laju .ndap Darah 9L.D: " G &* 9mm8jam:

    Diff count / Hitung Jenis eu!osit

    Basofil " % & 9@:

    .osinofil " & 2 9@:

    Batang " ( 9@:

    Segmen " *% +% 9@:

    Limfosit " (% ,% 9@:

    Monosit " ( ) 9@:

    !rinalisa

    Aenis Spesimen " urine midstream 8 porsi tengah

    !rine Lengkap

    Earna " kuning

    Kejernihan " jernih

    1lukosa " negatif

    Biliru3in " negatif

    Keton " negatif

    Berat jenis " &'%%2 &'%2%

    Darah samar " negatif

    pH " * )

    Protein " negatif

    !ro3ilinogen " %'& &'% 9.!8dl:

    #itrit " negatif

    .sterase leukosit " negatif

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    Sedimen

    Leukosit " % 2 98LPB:

    .ritrosit " % & 98LPB:

    Silinder " negatif 98LPK:

    .pitel " F&

    Kristal " negatif

    Lain-lain " negatif

    Kimia Darah

    1lukosa # " )% &%% 9mg8dl:

    1lukosa PP " &%% - &(% 9mg8dl:

    1lukosa S " G &*% 9mg8dl:

    Kolesterol total " G (%% 9mg8dl:

    Trigliserida " G &*% 9mg8dl:

    HDL Kolesterol " < * 9mg8dl:

    LDL kolesterol " G &*% 9mg8dl:

    !reum " &* ,% 9mg8dl:

    Kreatinin " %'* &'* 9mg8dl:

    $sam urat " (', *'+ 9mg8dl:

    Biliru3in total " %'( & 9mg @:

    Biliru3in direk " % %'( 9mg @:

    Biliru3in indirek " %'( %') 9mg @:

    S1/T " * ,% 9u8l:

    S1PT " * ,& 9u8l:

    $lkali osfatase " ,* &C% 9iu8l:

    1amma 1T " , &) 9mu8ml:

    Protein total " '& )'( 9gr @:

    $l3umin " 2') *'% 9gr @:

    1lo3ulin " ('2 2'( 9gr @:

    &. Teori !e'adian (atofisiologi (oli(

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    Pem3entukan polip sering diasosiasikan dengan inflamasi kronik5 disfungsi saraf

    otonom serta predisposisi geneti4' Menurut teori Bemstein5 terjadi peru3ahan mukosa

    hidung aki3at peradangan atau aliran udara yang 3ertu3ulensi5 terutama di daerah sempit

    di kompleks ostiomeatal' Terjadi prolaps su3mukosa yang diikuti oleh reepitelisasi dan

    pem3entukan kelanjar 3aru' Auga terjadi peningkatan penyerapan natrium oleh

    permukaan sel epitel yang 3eraki3at retensi air sehingga ter3entuk polip' Teori lain

    mengatakan karena ketidak seim3angan saraf ?asomotor terjadi peningkatan

    permea3ilitas kapiler dan gangguan regulasi ?as4ular yang mengaki3atkan dilepasnya

    sitokin-sitokin dari sel mast5 yang akan menye3a3kan edema dan lama-lama menjadi

    polip' Bila proses terus 3erlanjut5 mukosa yang sem3a3 makin mem3esar menjadi polip

    dan kemudian akan turun ke rongga hidung dengan mem3entuk tangkai'

    Pem3entukan polip sering dihu3ungkan dengan proses inflamasi kronik5 disfungsi

    sistem saraf otonom dan predisposisigenetik' Be3erapa teori telah dikemukakan5 tetapi

    tidak ada satupun yang dapat menjelaskan patofisiologi polip hidungse4ara lengkap'

    Menurut teori Bernstein5 inflamasi pertama terjadi di mukosa dinding lateral hidung atau

    mukosa sinusse3agai aki3at dari peradangan oleh alergan5 polutan5 atau agen infeksius

    9?irus 8 3akteri: atau karena adanya aliran udarayang 3ertur3ulensi' Pada se3agian 3esarkasus5 polip 3erasal dari area sempit di kompleks ostiomeatal 9K/M: di meatusmedia'

    Terjadi kerusakan atau prolaps mukosa yang diikuti dengan reepitelisasi dan

    pem3entukan kelenjar 3aru' Selamaproses terse3ut polip dapat ter3entuk dari mukosa

    karena proses inflamasi dari sel epitel5 sel endotel pem3uluh darah5 danfi3ro3last

    3erpengaruh pada integritas 3ioelektik natrium 4hannel pada mukosa hidung' Hal ini

    menye3a3kan meningkatnyaa3sorpsi natrium sehingga terjadi retensi air dan

    pem3entukan polip'Pada teori kerusakan epitel menjelaskan 3ah7a rusaknya epitel pada

    mukosa hidung dise3a3kan karena dalam keadaansakit 9alergi5infeksi: terjadi

    peningkatan turgor jaringan' Kerusakan terse3ut menye3a3kan prolaps lamina propia

    mukosasehingga terjadi pem3entukan polip yang dapat 3ertam3ah ukurannya karena efek

    gra?itasi atau o3struksi ?ena yangdise3a3kan polip'Dari penelitian ditemukan 2+@ pasien

    fi3rosis kistik menderita polip hidung' i3rosis kistik adalah penyakit herediter autosomal

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    resesif yang dise3a3kan karena adanya kerusakan pada gen 4ysti4 fi3rosis transmem3rane

    regulator 9T: dikromosom +' 1en ini mengatur 4hloride 4hannel pada sel epitel pada

    3er3agai organ5 termasuk saluran nafas' Kerusakanpada gen ini menye3a3kan

    terganggunya pem3ersihan sekret dan dihasilkannya sekret kental yang dapat

    menye3a3kano3struksi dan merupakan predisposisi infeksi pada paru-paru dan sinus

    paranasal

    Introduction

    During the past century several theories have been proposed to

    explain the etiopathogenesis of nasal polyposis. The fact that so many

    theories have been proposed is the evidence of our poor knowledge of

    this topic. Majority of these theories are based on tissue oedema,

    increase in the number of tubulo-alveolar glands, presence of cysts of

    mucous glands.

    Adenoma fibroma theory of Billroth:

    illroth in his studies found a large number of tubular glands in the

    nasal polypoidal tissue studied. !e concluded that these glands were

    not normally seen in such large numbers in the nasal mucosa. !e

    hence interpreted nasal polyp to be adenomas that began growing

    under the nasal mucosa pushing the epithelium and nasal glands

    outwards. !owever !opmann disagreed with this hypothesis saying

    that the glandular tissue found in the tissue samples of nasal polypi

    studied contained only mucous glands normally found in the nasalmucosa and concluded that nasal polypi could be soft fibromas and

    used the term fibroma theory to explain this. These two theories are

    not currently accepted at present.

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    "igure showing increase in the number of nasal mucosal glands

    "igure showing development of nasal polypi due to increase in the number

    of nasal mucosal glands #$denoma theory%

    Necrotizing ethmoiditis theory of Woakes:

    This theory suggests that ethmoiditis causes periostitis and ostitis of

    ethmoid bone causing bone necrosis. The necrotic bone initiates mucosal

    reaction leading on to mucosal oedema and polyp formation. This theory

    has been flawed from the very begining as no evidence of bone necrosis

    could be found in the polypoidal tissue studied so far.

    Glandular cyst theory:

    &vidently this theory is based on the presence of cystic glands and

    mucous filled cysts in the nasal polypoid tissue. The probable cause for

    the formation of these glandular cysts could be oedema of submucosa

    causing obstruction to the drainage of mucoid glands present in the nasal

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    mucosa. These mucous cysts expands outwards pushing the nasal

    mucosa causing the polyp to occur. Taylor in his meticulous study has

    proved that mucous glandular cysts usually occur after the polyp has

    formed and hence he believed that glandular cysts could be caused by

    nasal polyposis and not vice versa.

    Mucosal exudate theory of Hayek:

    !ayek beleived that nasal polyp formed due to accumulation of exudate

    localised deep in the mucosa. This accumulation of exudate causes the

    mucosa to bulge leading to polyp formation. 'asal mucosal glands and

    tubuloalveolar glands are also

    displaced outwards. These glands are hence found in the distal part of the

    polyp.

    Theory of cystic dilatation due to obstruction of excretory ducts of nasal

    glands and blood vessel obstruction(

    "igure showing cystic enlargement of nasal mucosal glands

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    "igure showing cyst formation prior to nasal polyposis

    )n chronic inflammation involving nasal mucosa blocks the excretory ducts

    of nasal tubulo alveolar glands causing the glands to dilate due to pent up

    secretions within. The blood vessels #capillaries and veins% surrounding

    these distending glands are also stretched. *tretching of these blood

    vessels impedes blood circulation and causes tissue oedema due to

    transudation of fluid. This theory is not valid due to the fact that dilatation

    of mucous glands occur only after formation of nasal polypoidal tissue.

    Blockade theory of Jenkins:

    This theory is based on the premise that development of nasal polypi is

    almost always preceded by certain degree of nasal mucosal inflammation.

    The inflammation could be the result of either infection + allergy.

    !istologically polyp itself is accumulation of intracellular fluid dammed up

    in a localied tissue. )f this blockage persists polyp develop, if the

    blockage covers a large area then multiple polypi forms. This theory

    doesnt explain why nasal polyp prefers certain areas of nasal cavity.

    eri!hlebitis " !erilym!hangitis theory of #ggston and Wolff:

    This theory is based on the premise that recurrent infections of nasal

    mucosa blocks intercellular fluid transport mechanism in the mucosa. This

    is always associated with oedema of lamina propria. This theory is based

    on the demonstration of chronic vascular changes in the nasal mucosa in

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    response to inflammation. !istologically these changes are supposed to

    be rather diffuse and hence cannot be used to explain the pathogenesis of

    nasal polypi which can always be localised to certain areas of nasal cavity.

    Glandular hy!er!lasia theory of $ra%ina:

    $ccording to rajina chronic inflammation of nasal mucosa cause local

    hyperplasia of nasal mucosal glands. These hyperplastic glands will cause

    bulging of nasal mucosa. )n addition to glandular hyperplasia changes that

    occur in the blood vessels will cause oedema in the region of the middle

    meatus. This in turn increases nasal mucosal oedema. *tudies have

    shown that the number of nasal mucosal glands are the same in

    polypoidal as in the normal tissue.

    #!ithelial ru!ture theory:

    This is the currently proposed theory. )n this theory the initial stage of

    nasal polyp formation starts of as epithelial rupture possibly due to

    inflammation and tissue oedema. This is followed by prolapse of lamina

    propria through the defect. The adjacent epithelium attempts to cover up

    the defect there by forming a lining for the polypoidal tissue. )f the defectin the epithelium is not covered up real fast the prolapsed lamina propria

    continues to grow and the polyp complete with its stalk develops. $fter

    epitheliation of the polyp the characteristic new long tubular glands are

    formed.

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    "igure showing &xudate forming under the nasal mucosa #&xudative

    theory%

    "igure showing nasal polyp forming after accumulation of exudate

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    "igure showing rupture of epithelium

    "igure showing development of nasal polyp following epithelial rupture

    &ole !layed by mucous glands:

    The glandular elements seen in the nasal polypoidal tissue are nasal

    glands. ommonly seen glands are degenerated long glands. The entire

    long duct along with their lateral branches are distended due to filled upsecretions. Due to the pent up secretion and distention the secretory

    epithelium of the nasal gland become cuboidal and flat losing their

    secretory ability. This is followed by degeneration of the gland.

    &ole !layed by cellular infilatrates:

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    &osinophilic infiltration is an important feature in the pathogenesis of

    chronic rhinosinusitis and nasal polypi. $ccumulation of eosinophils in the

    polyp stroma is basically caused by increased transendothelial migration,

    increased survival, and increased concentration of interleukin /.

    ). Per*edaan r#initis alergi+ r#initis ,asomotor+ r#initis medicamentosa dan r#initis

    infe!si

    hinitis

    akut

    hinitis kronik hinitis spesifik

    hinitisSimplek

    hnitishipertrofi

    hnitissika

    hinitisalergi

    musiman

    hinitisalergi

    tahunan

    hinitis?asomotor

    hinitismedikamento

    sa&tiologi

    -hino?irus-Myo?irus-0irus4oasa4kle

    -0irus.H/

    Infeksi

    3erulang

    dalam

    hidungdan sinus

    -/rangtua

    yang

    3ekerja

    di luarruangan

    -Penderita

    anemia

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    an yang

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    nya

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    Se4ret4air

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    serous

    Se4retmukoid

    0ejala Demamdan panas

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    Hidung

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    n

    Tes kulit 9-: