KARSINOMA PARU CA PARU dr Retna Dwi Sp

KARSINOMA PARU (CA PARU) dr. Retna Dwi, Sp. P SMF/LAB ILMU PENYAKIT PARU RSD. DR. SOEBANDI FAKULTAS KEDOKTERAN UNIVERSITAS JEMBER 2017

KARSINOMA BRONKOGENIK BATASAN : TUMOR GANAS PARU PRIMER YANG BERASAL DARI SALURAN NAFAS

TYPES OF LUNG CANCER l Non-Small Cell (NSCLC) 80% » Adenocarcinoma 40 -50% » Squamous Cell 20 -30% » Large 5 -10% l Small Cell (SCLC) 15 -20%

WHO : LEVELS of PREVENTION PRIMER : PREVENSI ELIMINASI / BLOCKING KARSINOGEN l SEKUNDER : DIAGNOSA DINI l TERTIER : TERAPI KURATIF l QUARTER : PENANGANAN PALIATIF l

WHO LEVELS of PREV in NSCLC I II IV CARCINOGEN AVOIDANCE EARLY DIAGNOSIS CURE PALLIATION & SUPPORTIVE +++ ? ? ++

EARLY DIAGNOSIS ? ? l IMAGING: 5 mm 3 = 32 x TUMOR DBL(s) l (1 cm 3 = 10^9 SEL) NATURAL COURSE DEATH : 40 x TUMOR DBL(s) 80 %COURSE of DISEASE NO MARK IMPACT on SURVIVAL ? ?

CURE DISAPPOINTING

PREVENTION

RELATIONSHIP TOBACCO – LUNG CA TUMOR SUBTYPE SQ. CELL CA % > 95 % SMALL CELL CA 90 % LARGE CELL CA 80 % ADENO CA 70 %

Tobacco use accounts for more than one-third of all cancer deaths. American Cancer Society, Cancer Facts & Figures, 2000

Smoking-Related Cancers • • • Bladder Cervical Esophageal Kidney Laryngeal • • Lung Mouth Pancreatic Throat

BILA ANDA : …. . l TIDAK MEROKOK JANGAN MULAI MEROKOK l MEROKOK DAN TETAP SEHAT USAHAKAN BERHENTI l MEROKOK + PENYAKIT AKIBAT ROKOK NON KANKER l MEROKOK + KANKER Sbg bentuk TANGGUNG JAWAB SOSIAL STOP ROKOK TETAP BERMANFAAT

SOCIAL RESPONSIBILITY Forced smoking

WORK UP

TATA LAKSANA l KECURIGAAN : » » » LAKI : ratio LK / W = 5: 1 USIA > 40 TH : 84. 2 % (Sby) PEROKOK : > 80 % PAPARAN INDUSTRI GEJALA KLINIK : – – BATUK >2 Mgg, BATUK DARAH, SESAK, BB TURUN > 4 kg/6 bln EXPERTISE DOKTER UMUM

KONFIRMASI / SKRINING X-RAY (+) X-RAY (-) CYTOLOGY (+) A B CYTOLOGY (-) C D A/B/C RUJUK l D : SKRINING ULANG BL INDIKASI TETAP ADA / 4 -6 bln l

NSCLC DIAGNOSIS Physical examination Detect signs Chest X-ray Detect position, size, number of tumors Bronchoscopy Precise location of tumor obtain biopsy FNA Cytology CT scan Detect chest wall invasion mediastinal lymphodenopathy distant metastases PET scan Lymph node staging Laboratory analysis Detect changes in hormone production, and hematological manifestations of lung cancer Mediastinoscopy Visualize and sample mediasturial lymph nodes NCCN Guidelines 2000

GAMBARAN KLINIK INTRA-PULMONAL INTRA - TORAKAL EKSTRA - PULMONAL GANGG. MUCUCIL ULSERASI OBSTRUKSI RADANG MEDIASTINAL INVOLVEMENT GEJALA EKSTRA-TORAKAL NON - METASTATIK NEUROMUSK. ENDOKRIN JAR. IKAT & TLG VASKULER METASTATIK

GEJALA INTRAPULMONAL l l BATUK LAMA / BERULANG : 70 -90% BATUK DARAH : 6 - 51% NYERI DADA : 42 -67% SESAK NAFAS : 58% MEKANISME : GANGG. GERAKAN SILIA, ULSERASI MUKOSA, RADANG BERULANG, OBSTRUKSI SAL. NAFAS

INTRATORAKAL EKSTRAPULMONAL PENYEBARAN TUMOR KE MEDIASTINUM : N. FRENIKUS : ---->DIAFR. N. REKURENS : ---->CH. VOCALIS S. SIMPATIK : ---->Sindr. HORNER ESOFAGUS : ----> DISFAGI V. CAVA SUP. : ----> Sindr. V. C. SUP. JANTUNG : ----> Gg. FUNGSI

EKSTRA PULM. NON METASTATIK l NEUROMUSKULER: » Myo / Neuro / Encephalopathia l ENDOKRIN & METABOLIK: » Syndr. Cushing / IADH / Karsinoid » gynecomastia / hyperpigmentasi l JAR. IKAT dan TULANG: » Clubbing fingers l VASKULER & HEMATOLOGIK » Anemia / purpurae / thrombo-phlebitis

METASTATIK EKSTRAPULMONAL l SATU-SATUNYA TUMOR yang mampu LANGSUNG AKSES ke SIRKULASI ARTERIIL l terutama : OTAK, HATI dan TULANG

SESAK PREV. 29 -74%, tergnt: JENIS & STADIA ETIOLOGI: l PENYAKIT PENYERTA a. l. : » PPOK, ASMA, DEKOMP. , ANEMI dsb l KOMPLIKASI / PENY. SUPERIMPOSED a. l. : » INFEKSI, EMBOLI PARU, ATELEKTASIS, PNEMOTORAKS, EFUSI PLERA dsb l l KANKER PARU nya sendiri IATROGENIK a. l. : » akibat RADIASI, akibat KEMOTERAPI (misalnya FIBROSIS o. k. BLEO. ) , akibat PEMBEDAHAN

FARMAKOLOGIK BRONKODIL. STEROID RADIASI R. STIMULAN OKSIGEN R. DEPRESS. SESAK FISIOTERAPI KEMO KHUSUS: stent

BATUK FREKW. : + 83 % KANKER PARU l PATOFISIOLOGI: l » PRODUKSI MUKUS BERLEBIH » INHALASI BENDA ASING / TERSELAK » STIMULASI ABN. PUSAT BATUK l PRINSIP PENANGANAN: » KAUSAL » V/S Faktor REVERSIBEL » SIMPTOMATIS » SUPORTIF

INFEKSI OBSTRUKSI STEROID SUPRESAN NEBUL. ANEST FISIOTx ANTIBIOT. SUPRESAN EKSPEKT. FISIOTx BATUK REFLUKS ESOF. ASPIRASI POSISI TEGAK ANTI REFL. ANTI-KHOL NEB. ANEST

BATUK DARAH l l l SELALU PATOLOGIK JARANG ASFIKSIA atau EKSANGUINASI STRESS : MENGINGATKAN akan KANKERNYA serta PROGRESIFITAS FREKW. KANKER PARU 47 - 70 % PENANGANAN : » SUPRESI BATUK » HEMOSTATIK v/s OOZING KAPILER » KEMOTERAPI, RADIASI dan LASER

NSCLC stages Lymph nodes Invasion of chest wall Metastasis to distant organs Main bronchus Stage 0 Stage IA Stage IIB Contralateral lymph node Stage IIIB Stage IV

TNM DEFINITION in NSCLC T PRIMARY TUMOR TX RO / FOB VISUALIZATION (-); MALIGN. CELLS in BRONCHIAL SECRETIONS (+) T 0 NO EVIDENCE OF PRIMARY TUMOR TIS CARCINOMA INSITU T-1 < 3 cm, SURROUNDED BY LUNG or VISCERAL PL; w. o. INVASION PROX to a LOBAR BR. T-2 Ø 3 T-3 l. DIRECT T-4 l. INVASION cm or INVADES VISC. PL or ATELECT(+) or OBSTRUCT. PNEUMONITIS extending TO HILAR, but < ENTIRE LUNG Ø. FOB > 2 cm from CARINA EXTENSION into CHEST WALL; DIAPHR. , MEDIAST. PL, PERICARDIUM, PANCOAST, w. o. INVOLVING HEART, GREAT VESSELS, TRACHEA, CORP. VERT. l. FOB < 2 cm from CARINA of MEDIAST INVOLVING ABOVE STRUCTURES l. MALIGNANT PL. EFFUSION

TNM DEFINITIONS in NSCLC N NODAL INVOLVEMENT N-0 REGIONAL LY. ND (-) N-1 LY ND PERIBRONCHIAL / IPSILATERAL HILAR(+) N-2 LY ND IPSILATERAL MEDIAST; SUBCARINAL(+) N-3 LY ND CONTRALATERAL MEDIAST / HILAR; SCALENE / SUPRA CLAV (+)

TNM DEFINITIONS in NSCLC M DISTANT METASTASIS M-0 NO (KNOWN) DISTANT METASTASIS M-1 DISTANT METASTASIS (+) RECOMMENDATION : SPECIAL CASES PERICARDIAL EFF. : T-4 N. PHRENICUS : T-3 N. LARYNGUS REC : T-4

SCLC staging Extensive: Tumor not confined to hemithorax of origin Distant metastasis Limited: Tumor confined to hemithorax of origin and/or the mediastinum and supraclavicular nodes PDQ Guidelines 2000

STAGING SCLC LIMITED DBL AMAT CEPAT EXTENSIVE BATAS : SUDAH / BELUM TERLAMPAUI IPSILATERAL HILAR NODES TX NON SURGICAL CHEMO SURV ; CURE(-)

TREATMENT

TERAPI l UMUM : 5 MODALITAS TERAPI 1. PEMBEDAHAN 2. SITOSTATIKA WHO 3. RADIASI 4. HORMONAL (NSCLC) 5. IMUNOLOGIK EXPERIMENTAL

PENENTUAN MODALITAS TERAPI HISTO PATH SURGERY CHEMO / & RADIASI HORMONAL BIOLOGICAL RESPONSE MODIFIER (BMR) GENE TX NSCLC SURGICAL CASE CURATIVE? PALLIATIVE ? SCLC NON SURGICAL MAIN THERAPY ?

SURGERY

TNM STAGING NSCLC N-0 N-1 N-2 N-3 T-1 IA III B T-2 IB III A III B T-3 II B III A III B T-4 III B ALL M-1 = IV OPERABLE

SURGICAL OPTION: MAJOR CONSIDERATIONS FITNESS for SURGERY 1. AGE 2. PULM. FUNCTION 3. CARDIOVASC. FITNESS 4. NUTRITION & PERFORMANCE STATUS OPERABILITY 1. DIAGNOSIS & STAGING 2. ADJUVANT THX. 3. SURG. PROCEDURES AVAILABLE 4. LOCALLY ADV. DISEASE 5. SMALL C. L. C.

CHEMO THERAPY

KEMOTERAPI PERSYARATAN : PERFORMANCE : KARNOFFSKY > 70 = ECOG / WHO 0 -1 l MEMAKSAKAN KEMOTERAPI PADA KONDISI YANG TIDAK MEMENUHI SYARAT MEMPERCEPAT KEMUNDURAN PENDERITA

SKALA TAMPILAN (PERFORMANCE SCALE)

CHEMOTHERAPY REQUIREMENTS l l KARNOFFSKY > 70 / ECOG 0 -1 -(2) WEIGHT LOSS < 10 % l TRUTHFUL INFORMATION Do NOT give FALSE HOPE Do NOT DESTROY HOPE

BIOLOGIC TREATMENT TARGETTED THERAPY

Combinations of Chemotherapy and Biologic Therapy : A New Paradigm for the 21 st Century

EGFR SIGNALING NETWORK

FINAL OBJECTIVE Might not lengthen survival, B U T increase their QUALITY OF LIFE Attaining A Meaningful survival

Time flies