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Dr Sumardi PPOK_Emfisema-UII
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PENYAKIT PARU OBTRUKTIF KRONIK (PPOK)
Bronkitis kronis
Batuk + dahak kumat2-an lebih dari 2 tahun oleh karena merokok atau polusi
Emfisema
Sesak nafas + batuk kumat2an lebih dari 2 tahun oleh karena merokok atau polusi
EMFISEMA• Klinis: dyspnea keadaan istirahat, dada
cembung (tong chest), hipersonor, sianotik, jari tabuh.
• CXR: hiperlusen, diafragma datar• Kelainan utama pada cabang bronkus
terminal yg. berhubungan dengan alveoli• Septa alveoli rusak luas alveoli
inefisiensi pertukaran gas• Kerusakan septa o.k. elastase yang
dihasilkan netrofil lebih tinggi dari alfa-1 antitripsin yg melindungi integritas alveoli
• Kerusakan bersifat irreversibel
Emphysema. PA Chest radiography in a patient with severe emphysema secondary to alpha-1 antitrypsin
deficiency
Emphysema. Graphic depiction of centrilobular versus panlobular emphysema
Pathology …. 13 (normal parenchyma)
Pathology …. 14 (emphysema)
Pathology …. 15
Pathology …. 16 (normal small airway)
Pathology …. 17
“Small Airways Dysfunction”
Flow
Volume
Expiratory flow limitation
On forced exhalation
During exercise
At rest
Bronchus
Wall thickening – inflammation -- mucus gland hypertrophy
↑ Secretions
Alveoli
Wall thinning - inflammation - elastolysis
Coalescence
↓ Elasticity
Bronchiole
Wall thickening – inflammation – repair -- remodeling
Loss of alveolar attachments
Airway
Resistance
Normal Central Air way Obst.
Small Air-way Obst.
Central 80 160 80
Peripheral 20 20 40
R total 100 180 120
Silent Zone
COPD and the Distribution of Airway
Resistance
Large airway
Small airway
COPD Pathology and Abnormal Breathing Mechanics
• ↑ Airway resistance • ↓ Elastic recoil • Expir. flow limitation• Air trapping and
dynamic hyperinflation• ↑ Work of breathing• Dyspnea, cough and
other respiratory ssx• ↓ Quality of life
Pathology of Breathing Peripheral Lung Zone
• Airways open and not prone to collapse low resistance
• Lung recoil strong enough to drive tidal expiration (passive)
• Work of breathing is minimal
Pathology:Altered Lung Mechanics
• Airway wall thickened and collapsing high resistance
• Alveoli thinned out poor elastic recoil
• Expiratory flow limitation
• Residual volume increased
Thin-section CT scan of a Smoker
End-inspiration End-expiration
Pathology …..
Pathology …..
Pathology …..
PPOK
Eksaserbasi Akut
1. Batuk + dahak berlebihan
2. Dahak berubah warna kuning,hijau,bau
3. Demam tanda infeksi
4. Sesak nafas memberat (emfisema)
PPOK Eksaserbasi Akut
Manajemen:1. Istirahat + O2 2-3 liter/menit2. Diet tinggi kalori,tinggi protein, rendah karbohidrat3. Antibiotika: makrolid, kuinolon, penisilin4. Steroid oral: metil prednisolon, prednison 40-60
mg/hari 7-10 hari5. Steroid inhalasi: budesonid/flutikason 1-2 mg/hari6. Bronkodilator inhalasi: salbutamol/terbutalin 600-
1200 mcg/hari+Ipatrium bromid (Combivent)7. Aminofilin lepas lambat 200-400 mg 2x/hari8. Mukolitik: N asetil sistein, ambroksol, OBH, GG
SUMMARY
• OXYDATIVE STRESS INFLAMATION• INCREASE CYTOKINE + CHEMOKINE• IMBALANCE PROTEASE-ANTIPROTEASE• MUCOUS SECRETION• REMODELLING SMALL AIRWAY• PARTIALLY IRREVERSIBLE IRREVERSIBLE
• OBSTRUCTION AIRTRAPPING• DESTRUCTION PARENCHYMA EMPHYSEMA