[09-10] (IPD) Kelainan Rongga Mulut Dan Esofagus

7/27/2019 [09-10] (IPD) Kelainan Rongga Mulut Dan Esofagus

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DIVISI GASTROENTEROLOGI-HEPATOLOGI

DEPARTEMEN ILMU PENYAKIT DALAM

FK-USU/RSUP H.ADAM MALIK MEDAN

Kelainan rongga mulut dan Esofagus

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Learning Object

K-8

Kelainan rongga mulut (Disorders of the mouth)

Herpes stomatitis. Oral thrush,

Acute necrotizing ulcerative gingivitis.

Kelainan pada Oesophagus :

Odinofagia. Disfagia

K-9 :

Kelainan pada Oesophagus :

Gangguan pasase oesophagus.

Striktura oesophagus

Varises oesophagus

Gangguan motilitas oesophagus /reflux

oesophagitis.

Corosive lesions of oesophagus 2


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Kelainan rongga mulut:

Rongga mulut & mukosanya adl.target dari

berbagai penyebab infeksi, bahan kimia,dan bahan fisikal,dipengaruhi berbagaipenyebab peradangan pada mulut atau bgndari penyakit sistemik.

Beberapa hal yang perlu diketahui antara lain

Herpes stomatitis. Oral thrush,

acute necrotizing ulcerative gingivitis

Dll. 3


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HERPES STOMATITIS :

Lokasi : pipi, tongue, gingiva or palatum. Gambaran Klinis :

Erupsi vesicular unilateral & ulserasi linear sesuai

distribusi of n. Trigeminus atau cabangnya. Perjalanan penyakit : sembuh tanpa parut bila

tidak ada infeksi; bisa dijumpai post herpetic

neuralgia.

Oral acyclovir, famcyclovir, or valacyclovir

memperpendek masa penyembuhan and post

herpetic neuralgia.

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Investigation

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Tests are not usually necessary inimmunocompetent people, as history andexamination will usually confirm thediagnosis.

Viral culture from swabs of lesions has beenconsidered the gold standard but is limited by

the short time period of viral shedding andthe relatively low number of viral particlespresent in samples.


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Treatment

Topical antiviral agents: Aciclovir 5% can beused from the age of 3 months. Penciclovir1% cream should be used from the age of 12.

Treatment needs to be initiated at the onsetof symptoms before vesicles appear.

Topical antivirals need to be appliedfrequently for a minimum of 4-5 days.

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http://www.patient.co.uk/search.asp?searchterm=ACICLOVIR&collections=PPsearchhttp://www.patient.co.uk/search.asp?searchterm=PENCICLOVIR&collections=PPsearchhttp://www.patient.co.uk/search.asp?searchterm=PENCICLOVIR&collections=PPsearchhttp://www.patient.co.uk/search.asp?searchterm=ACICLOVIR&collections=PPsearch


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Aciclovir is active against herpes viruses butdoes not eradicate them. It can be used assystemic and topical treatment of herpessimplex infections of the mucous membranesand is used orally for severe herpeticstomatitis. Valaciclovir is an ester of aciclovir.

It is licensed for herpes simplex infections ofthe skin and mucous membranes.

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http://www.patient.co.uk/search.asp?searchterm=HUMAN+HERPES+VIRUSES&collections=PPsearchhttp://www.patient.co.uk/search.asp?searchterm=VALACICLOVIR+PRODUCT&collections=PPsearchhttp://www.patient.co.uk/search.asp?searchterm=VALACICLOVIR+PRODUCT&collections=PPsearchhttp://www.patient.co.uk/search.asp?searchterm=HUMAN+HERPES+VIRUSES&collections=PPsearchhttp://www.patient.co.uk/search.asp?searchterm=HUMAN+HERPES+VIRUSES&collections=PPsearchhttp://www.patient.co.uk/search.asp?searchterm=HUMAN+HERPES+VIRUSES&collections=PPsearch


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Referral

Seek advice for managing

immunocompromised individuals, includingpeople with HIV.

Seek specialist advice if neonatal herpes issuspected (rare; may present with skin, eyeand/or mouth symptoms).

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Oral thrush Lesi putih pada mukosa mulut.Tanda Klinis :

Tipe Pseudomembraneous (thrush) : daerah denganpenebalan lunak berwarna putih krim dalam bentukbarisan),permukaan berdarah bila dogosok.

Tipe Erythematous : datar, merah, terkadang area yang sakit

dalam kelompok yang sama

Candidal leukoplakia : Penebalan putih tidak dapat diangkat,

penebalan epitel disebabkan candida.

Angular cheilitis: fissures yang sakit pada sudut mulut.

Perjalanan penyakit : Respon baik dgn terapi antifungal koreksi faktor predisposisi.

Perjalanan sama dengan pseudomembraneous type.

Respon dengan pemberian terapi jangka lama antifungal.

Respon dengan terapi topical antifungal. 10


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Penyebab :

Pertumbuhan Candida dalam keadaan normal dikontrol oleh

adanya bakteri normal. Pertumbuhan berlebih dan tidak terkontrol pada mulut

disebabkan oleh faktor yang menurun kan resistensi natural,

misalnya sakit, stress, pemakaian lama corticosteroidsatau obat yang menekan immune system, dan kelainanimmune misalnya (HIV/AIDS).

Disebabkan keadaan yang mengganggu keseimbangannormal microorganisms dalam mulut :

kebanyakan akibat pemakaian lama antibiotik , & uncontrolled DM & dengan perubahan hormonal

akibat pregnancy atau penggunaan pil KB.

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Symptoms

Biasanya pada lidah, atau bgn dalam pipi.

Warna keputihan

Nyeri

- Mulut Kering.

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Pemeriksaan dan Tests candida.

Terlihat adanya area/lesi pada mulut,lidah, atau pipi.

Lesi mudah disikat dan terlihat area kemerahan,nyeri dan bisa berdarah.

Pemeriksaan mikroscopi jaringan lesi, dapatmemastikan infeksi Candida, tapi biasanyadiagnosis dibuat dengan simple physicalexamination

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Self - Care

Follow good oral hygiene practices. Brush the teeth atleast twice a day and floss at least once a day.

Avoid mouthwashes or sprays which can destroy thenormal balance of microorganisms in the mouth.

Visit dentist regularly. Especially for people with diabetesor wear dentures.

Limit the amount of sugar and yeast-containing foodsintake. (Bread, beer, and wine encourage candidagrowth).

Quit smoking.

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Treatment

For thrush in infants, treatment is often NOT needed. Itusually gets better on its own within 2 weeks.

Use a soft toothbrush and rinse your mouth with adiluted 3% hydrogen peroxide solution several times aday.

An antifungal suspension (nystatin) can be use for severecase of thrush. These products are usually used for 5 - 10days.

Stronger oral medications such as fluconazole oritraconazole may be use if the infection has spreadthroughout the body or in a weakened immune systemauch as HIV/AIDS.

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Prognosis:

Menggangu proses makan,karena rasa tidakenak/sakit.

Biasanya respon dgn pengobatan, tapi bisakambuh kembali.

Dapat meluas ke palatum, lidah, pipi,atautenggorok.

Penyebaran ketempat lain bisa terjadi walautidak umum

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KOMPLIKASI :

Gangguan nutrisi. Esophagitis Candida

Penyebaran candida ke saluran cerna, paru,

kulit,dan area lainnya.

PENCEGAHAN :

Penderita yang sering kambuh, atau risiko tinggiuntuk terjadi oral thrush, bisa diberi profilaksis.

(preventive) antifungal medications.

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ACUTE NECROTIZING ULCERATIVE GINGIVITIS

(Trench mouth, Vincents infection):

lokasi biasanya : Gingiva.Gambaran klinis : sakit, perdarahan gingiva

ditandai dengan necrosis and ulserasi gingivalpapillae dan pinggirnya

Disertai lymphadenopathy dan bau mulut.

Terapi : debridement dan larutan

peroxide, akan mengatasi keluhan dlm 24 jamantibiotik pada yg akut

Bisa terjadi relaps.

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Management

Includes local debridment ( ultrasonicscaling), subgingival curettage and use ofmild oxygenating solutions.

Antibiotic thereby includes penicillins orerythromycin and metronidazole.

NSAIDs may be used for pain relief.

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Kelainan pada Esofagus

Odinofagia.

Disfagia

Gangguan pasase oesophagus. Striktura oesophagus

Varises oesophagus

Gangguan motilitas oesophagus /reflux

oesophagitis.

Corosive lesions of oesophagus

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Kelainan Esofagus

Dysphagia:( Disfagia)

Kesulitan menelan.

Odynophagia:

Painful swallowing, is characteristic of nonrefluxesophagitis (particularly monilial), herpes, and pill-induced esophagitis.

may occur with peptic ulcer of the esophagus(Barrett's ulcer),carcinoma with periesophagealinvolvement, caustic damage of the esophagus,and esophageal perforation

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Kelainan esofagus

Phagophobia : rasa takut menelan, dan menolak untukmenelan.

Bisa terjadi pada hysteria, rabies, tetanus, dan paralysisfaring.

Aphagia : obstruksi esofagus yg komplit,biasanya akibatsangkutnya bolus dan merupakan suatu darurat medik.

Globus pharyngeus/globus sensation(globus hystericus) :

perasaan adanya gumpalan yang mondok dikerongkongan,tapi tidak ada kesulitan menelan.Dijumpai kontinu tapi tdk berhubungan dgn menelan.Bisa hilang sementara waktu menelan.

Penyebab umum globus sensation :

( GERD,anxiety disorder, Early hypopharyngeal cancer,goiter.

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Heartburn, or pyrosis

ditandai rasa terbakar retrosternal, rasa tidak

enak, bisa menjalar keatas/kebawah dada, spt

gelombang.

- Bila berat, bisa menjalar kesebelah dada,leher,dan sudut rahang.

- Heartburn adl. Keluhan khas dari reflux

esophagitis dan bisa berhubungan dengan

regurgitation rasa adanya cairan hangat naikketenggorok. Akan bertambah berat bila ada

tekanan, atau berbaring dan makin berat

sesudah makan.

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Causes of dysphagia

Diseases of the mouth and tongue e.g. Tonsillitis

Neuromuscular disorders e.g. bulbar palsy,

myasthenia gravis

Motility disorders e.g. achalasia, scleroderma,diffuse esoph. Spasm

Intrinsic lesions e.g. ,strictures (benign/malignant),

esoph. web/ring

Extrinsic pressure e.g. goiter, pharyngeal pouch,

aortic aneurysm, enlarged left atrium

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Dysphagia : adl kesukaran dalam menelan.

Biasanya os mengeluh makanan tersangkut antara

mulut, faring atau esofagus.

salah arah dari makanan menyebabkan nasalregurgitation, laryngeal dan aspirasi paru waktumenelan, merupakan tanda khas dari oropharyngealdysphagia.

Lesi peradangan yang sakit yg menyebabkanodynophagia bisa juga menyebabkan penolakanuntuk menelan.

Ada pasien yang dapat merasakan turunnya makananke esophagus. Sensitifitas seperti ini tidakberhubungan dgn suatu food sticking atau obstruksi.

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Patofisiologi Disfagia

Tergantung pada lokasi anatomidibagi atas

disfagia oral,faringeal dan esofagial.

Transport bolus tergantung pada : ukuran bolus &

lumen, kontraksi peristaltik, relaksasi normal dari

UES dan LES selama menelan.

Disfagia ok bolus yg besar atau lumen sempitDisfagia mekanis (mechanical dysphagia)Akibat lemahnya kontraksi peristaltikmenyebabkan kontraksi non peristaltik dangangguan relaksasi sfinkter disbt: motor dysphagia.

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Disfagia orofaringeal :

Fase oral disfagia, adl berhubungan dgnpembentukan bolus yg jelek,makanan keluarmulut atau tinggal di mulut atau os merasa sulit

memulai refleks menelan.

Kontrol bolus yg jelek-makanan ke dalam faringdan aspirasi ke laring dan/atau rongga hidung.

Fase faring disfagia : ok statis makanan dlm faringakibat prepulsi faring yg jelek dan obstruksi padaUES.

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Dysfagia Orofaringeal

Stasis faring - nasal regurgitation & aspirasilaring selama dan setelah menelan.

Adanya regurgitasi nasal dan aspirasi laringselama menelan, adalah suatuhallmarks

dari disfagiaorofaring.

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Penyebab disfagia orofaringeal

Gangguan otot lurik-neurologik, miopati.

Lesi inflamasi mulut, faring dan laring.

tumor laring dan faring. Abses retrofaringeal

Divertikulum Zenker (kantung faringeal)

Goiter

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Oropharyngeal Mechanical Dysphagia


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Oropharyngeal Mechanical Dysphagia

I. Wall defects : A. Congenital: 1. Cleft lip, cleft palate 2. Laryngeal

clefts B. Post surgical

II. Intrinsic narrowing : A. Inflammatory

1. Viral (herpes simplex, varicella-zoster, cytomegalovirus)

2. Bacterial (peritonsillar abscess)

3. Fungal (Candida)

4. Mucocutaneous bullous diseases

5. Caustic, chemical, thermal injury .

B. Strictures 1. Congenital microganthia 2. Caustic ingestion

3. Post-radiation

C. Tumors 1. Benign 2. Malignant

III. Extrinsic compression A. Retropharyngeal abscess, mass B.Zenker's

diverticulum C. Thyroid disorders D. Vertebral osteophytes

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Oropharyngeal Motor Dysphagia


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Oropharyngeal Motor Dysphagia

I. Diseases of cerebral cortex and brainstem

A. With altered consciousness or dementia 1. Dementias including Alzheimer's disease

2. Altered consciousness, metabolic encephalopathy,

encephalitis, meningitis, cerebrovascular accident,

brain injuryB. With normal cognitive functions

1. Brain injury 2. Cerebral palsy

3. Rabies, tetanus, neurosyphilis

4. Cerebrovascular disease 5. Parkinson's disease and other extrapyramidal lesions

6. Multiple sclerosis (bulbar and pseudobulbar palsy)

7. Amyotrophic lateral sclerosis (motor neuron disease)

8. Poliomyelitis and post-poliomyelitis syndrome 35

Orofaringeal motor dysfagia


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Orofaringeal motor dysfagia

II. Diseases of cranial nerves (V, VII, IX, X, XII)

A. Basilar meningitis (chron inflammatory,

neoplastic)

B. Nerve injury

C. Neuropathy (Guillain-Barr syndrome, familial dysautonomia,

sarcoid, diabetic and other causes)III. Neuromuscular

A. Myasthenia gravis B. Eaton-Lambert syndrome

C. Botulinum toxin D. Aminoglycoside & other drugs

IV. Muscle disorders

A. Myositis (polymyositis, dermatomyositis sarcoidosis)

B. Metabolic myopathy (mitochondrial myopathy,thyroid myopathy)

C. Primary myopathies (myotonic dystrophy,

oculopharyngeal myopathy) 36

Esophageal dysphagia


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Esophageal dysphagia Penyakit intraesofagus :

Striktur jinak esofagitis refluks, esofagitis korosif,

trauma. Karsinoma

Rings dan webs

Gangguan motorik-akalasia, spasma difus, sklerosis

sistemik. Tekanan dari luar atau ekstrinsik :

Kelenjar dan tumor mediastinum.

Aneurisma

Pembesaran atrium kiri Dysphagia: penekanan esofagus oleh anomali arteri

subklavia kanan atau pbl. Darah besar lain.

Hernia hiatus paraesofageal (terputar).37


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Esophageal Dysphagia

Pd dewasa, lumen esofagus dapat distensi sp

diameter 4 cm. Bila esofagus tdk dapat dilatasi

melebihi diameter 2.5 cm -, dysphagia thd

makanan normal solid.

Dysphagia permanen terjadi bila esophagus

tdk dapat distensi melebihi 1.3 cm.(Critical

narrowing of the lumen for onset of dysphagia)

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Esofageal dysfagia


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Esofageal dysfagiaEsophageal Mechanical Dysphagia

I. Wall defects A. Congenital B. Tracheoesophageal fistula

II. Intrinsic narrowingA. Inflammatory esophagitis

1. Viral (herpes simplex, varicella- zoster, cytomegalovirus)

2. Bacterial 3. Fungal (Candida) 4. Mucocutaneous bullbous diseases

5. Caustic, chemical, thermal injury 6. Eosinophilic esophagitis

B. Webs and rings

1. Esophageal (congenital, inflammatory)

2. Lower esophageal mucosal ring (Schatzki's ring)

3. Eosinophilic esophagitis 4. Host-versus-graft disease

C. Benign strictures

1. Peptic 2. Pill-induced

3. Inflammatory (Crohn's disease, Candida, mucocutaneous lesions)

5. Ischemic,.Postoperative,. Post-radiation, Congenital

D. Tumors 1. Benign 2. Malignant 39


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Esofageal Dysfagia III. Extrinsic compression

A. Vascular compression ( left atrial enlargement, aortic aneurysm)

B. Posterior mediastinal mass C. Postvagotomy hematoma and fibrosis

Esophageal Motor Dysphagia

I. Disorders of cervical esophagus

II. Disorders of thoracic esophagus

A. Diseases of smooth muscle or excitatory nerves1. Weak muscle contraction or LES tone a. Idiopathic b.Scleroderma and related collagen

vascular diseases c. Hollow visceral myopathy d. Myotonic dystrophy e. Metabolicneuromyopathy (amyloid, alcohol?, diabetes?) f. Drugs:anticholinergics, smooth musclerelaxants

2. Enhanced muscle contraction a. Hypertensive peristalsis (nutcracker esophagus) b.Hypertensive LES, hypercontracting LES

B. Disorders of inhibitory innervation

1. Diffuse esophageal spasm 2. Achalasia a. Primary b. Secondary

3. Contractile (muscular) lower esophageal ring

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Tumor Esofagus

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Investigation Barium swallow or esophagram. This involves drinking a

fluid containing a barium compound that coats theesophagus and tumor so that they show up on x-ray. Ifthe stomach is also looked at, the test is called an uppergastro-intestinal series or upper G.I. series

Esophagoscopy This is performed by the surgeon or gastro-

enterologist (a specialist in stomach and boweldiseases)

Biopsy or removal of a small piece of the tumor iscarried out if a tumor is seen. This gives a definitediagnosis - noting whether there is malignancy or notand if malignant, what type of malignancy (squamouscell carcinoma or adenocarcinoma)

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CAT (computerized axial tomography) scan ofthe abdomen to determine whether or notthe cancer has spread to the liver or lymph

glands (nodes), which are common sites forspread of esophageal cancer

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Achalasia


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Esofagogram

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TERIMA KASIH

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[09-10] (IPD) Kelainan Rongga Mulut Dan Esofagus