TUGAS THT Nurul Jadi

8/13/2019 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 "

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2/16

&' 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(


8/16

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


9/16

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.


10/16

"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


11/16

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


12/16

"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


13/16

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.


14/16

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

theory%

"igure showing nasal polyp forming after accumulation of exudate


15/16

"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

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hinitisSimplek

hnitishipertrofi

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musiman

hinitisalergi

tahunan

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Tes kulit 9-:

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