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GOOD MORNING. JR IV. IMPACT OF ALCOHOL ABUSE IN THE ETIOLOGY AND SEVERITY OF COMMUNITY-ACQUIRED PNEUMONIA. Andres de Roux, Manuela Cavalcanti, Maria Angeles Marcos, Elisa Garcia, Santiago Ewig, Jose Mensa and Antoni Torres (Hospital clinic Barcelona, Spain). BY:
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JR IV IMPACT OF ALCOHOL ABUSE IN THE ETIOLOGY AND SEVERITY OF COMMUNITY-ACQUIRED PNEUMONIA Andres de Roux, Manuela Cavalcanti, Maria Angeles Marcos, Elisa Garcia, Santiago Ewig, Jose Mensa and Antoni Torres (Hospital clinic Barcelona, Spain) BY: DR. MEILAND TINA J. D. S SUPERVISOR : DR. H. ZAINUDDIN AMIR, SpP(K)
BACKGROUND ALCOHOL CONSUMPTION SYSTEMIC & PULMONARY IMMUNITY PULMONARY INFECTIONS
AIM OUTCOME ETIOLOGI COMPARE ALCOHOL ABUSE >< NONALCOHOLIC (HOSPITALIZED FOR CAP) SEVERITY OF DISEASES THE ANTIBIOTIC RESISTENCE OF STREPTOCOCCUS PNEUMONIAE
INTRODUCTION C A P MORBIDITY ↑↑ & MORTALITY↑↑ ADVANCES ANTIBIOTIC THERAPY
INTRODUCTION AGE TOXIC HABITS SEVERITY OF C A P IMMUNE STATUS COMORBIDITIS
INTRODUCTION TOXIC HABIT CELL MEDIATED IMMUNITY B LYMPHOCYTE ALCOHOL CONSUMPTION IMPAIRED FUNCTION PMN LEUKOCYTES DECREASED FUNCTION ALVEOLAR MACROFAG CYTOKINS
MATERIAL AND METHODS DEFENITIONS C A P SYMPTOMS CHEST Rö • COUGH • EXPECTORATION • CHEST PAIN • DYSPNOE • TEMPERATUR • BP • HR & RR LAB • NEW INFILTRAT • PLEURAL EFFUSION
MATERIAL AND METHODS DEFENITIONS ALCOHOL CONSUMPTION A PATIENTS NA PATIENTS EA PATIENTS • ♂>80 g/day • ♀>60 g/day • During the last • 2 years before HA • History (-) • ♂≤24 g/day • ♀≤12 g/day • History (+) • Abstained ≥ 1 yr
MATERIAL AND METHODS MICROBIOLOGICAL AG TEST CULTURE DIAGNOSIS SPUTUM PLEURAL FLUID URINARY BLOOD
MATERIAL AND METHODS PATIENTS Hospitalized w/ CAP Oct 1997- Nov 2001 (N=1.511) DATA INCLUDE (N=1.347) EXCLUDE (N=164) A PATIENTS (N=128) 10% EA PATIENTS (N=54) 4% NA PATIENTS (N=1.165) 86%
CONCLUSION • We found an independent association between pneumococcal infection and alcoholism. • Current alcohol abuse was associated with severe CAP • No significant differences were found in mortality, antibiotic resistance of S pneumoniae, and other etiologies.
PATOGENESA PROSES RADANG TERBAGI 4 TINGKAT: • Tingkat KONGESTI:(4-12 jam pertama) • Makroskopis : lobus paru yang terlibat berwarna kemerahan, membengkak, perabaan banyak cairan, pada irisan keluar cairan kemerahan. • Mikroskopis : kapiler melebar dan kongestif, alveolus terisi eksudat jernih (serous) dan bakteri dapat ditemukan dalam jumlahbanyak.
PATOGENESA • Tingkat HEPATISASI MERAH: (48 jam kemudian) • Makroskopis: lobus yang terlibat lebih padat, perabaan seperti hepar, irisan tampak kering, granuler dan berwarna merah. • Mikroskopis : netrofil ↑↑, tampak sel darah merah dalam alveolus. Eksudat berubah menjadi fibrinosa.
PATOGENESA • Tingkat HEPATISASI KELABU:(3-8 hari) • Makroskopis: perabaan masih tetap padat, hanya warna merah berubah jadi pucat-kelabu • Mikroskopis : sel-sel tampak kabur karena enzim proteolitik.Fibrin lebih menggumpal dan tampak amorf. Kuman tidak tampak lagi.Makrofag lebih berperanan dalam proses penyembuhan.
PATOGENESA • Tingkat RESOLUSI: (7-11 hari) • Makroskopis : paru-paru basah lagi dan pada irisan keluar cairan keruh. • Mikroskopis : eksudat yang melunak sebagian dibatukkan keluar, sebagian diabsorpsi. Dengan cara demikian seluruh kelainan dalam paru-paru akan kembali ke keadaan normal.
SISTEM IMUN Non-Spesifik Spesifik Fisik/Mekanik Larut Selular Humoral/ Sel B Selular/ Sel T • Mononuklear • (Monosit&Makrofag) • PMN • (Netrofil&Eosinofil) Ab • Sel Th • Sel Tst • Sel Tdh • Sel Tsup