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RESPIRATORY SYSTEM Department of Anatomic Pathology Faculty of Medicine Brawijaya University

RESPIRATORY SYSTEM Department of Anatomic Pathology Faculty of Medicine Brawijaya University. Tingkat Kemampuan 2

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RESPIRATORY SYSTEM Department of Anatomic Pathology Faculty of Medicine Brawijaya University

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  1. RESPIRATORY SYSTEMDepartment of Anatomic PathologyFaculty of MedicineBrawijaya University

  2. Tingkat Kemampuan 2 Lulusandoktermampumembuat diagnosis klinikterhadappenyakittersebutdanmenentukanrujukanbagipasienkepadaspesialis yang relevan. Lulusandokterjugaharusmampumenindaklanjutisesudahnya. Tingkat Kemampuan 3 3A. Lulusandoktermampumemberikanpenangananterhadappenyakittersebutpadakeadaan yang bukankeadaangawatdaruratsertamampumemberikanterapipendahuluandemimenyelamatkannyawaataumencegahkeparahandanataukecacatanpadapasien. Lulusandokterharusdapatmenentukanrujukanyang paling tepatbagipenangananlebihlanjutuntukpasiendanmampumenanganiperawatanselanjutnya.

  3. 3B. Lulusandoktermampumemberikanpenanganangawatdaruratpadapenyakittersebutdanmampumemberikanterpaipendahuluandemimenyelamatkannyawaataumencegahkeparahandanataukecacatanpadapasien. Lulusandokterharusdapatmenentukanrujukan yang paling tepatbagipenangananlebihlanjutuntukpasiendanmampumenanganiperawatanselanjutnya. Tingkat Kemampuan 4 Lulusandoktermampumenanganipenyakittersebutsecaramandiridantuntas. Merekaharusmampumenegakkan diagnosis pasienberdasarkanpemeriksaanfisikdanpemeriksaanpenunjang (misalnya: pemeriksaanlaboratoriumsederhanaatauX-ray) yang tepatgunadantidakberlebihan.

  4. KOMPETENSI Diagnosis  Rujuk Diagnosis  1st Treatment (Non Emergency)  rujuk Diagnosis  1st treatment (Emergency)  Rujuk Diagnosis  Appropriate Treatment

  5. DISEASES of RESPIRATORY SYSTEM • ATELECTASIS • COPD (EMPHYSEMA) • PULMONARY TUBERCULOSIS • LUNG CANCER • Definition • Pathophysiology • Macros • Micros • X-Ray • Clinical Appearance • Management

  6. ATELECTASIS

  7. What is it? # Atelectasis (at-uh-LEK-tuh-sis) is a condition in which one or more areas of lungs collapse or don't inflate properly. # Incomplete expansion of the lung (neonatal atelectasis) or collapse of previously inflated lung (acquired atelectasis), producing areas of relatively airless pulmonary parenchyma # Reversible

  8. Possible Underlying Disease Lung diseases such as COPD, asthma, cystic fibrosis, tuberculosis, and whooping cough also increase your risk for a collapsed lung

  9. Cause of Atelectase • Acquired atelectasis • resorption ( obstruction) atelectasis • compression atelectasis • contraction atelectasis

  10. Resorption atelectasis * Complete obstruction of an airway resorption of the oxygen trapped in the dependent alveoli lung volume diminished mediastinum shifts toward the atelectatic lung * Cause : excessive secretions (e.g., mucus plugs) or exudates within smaller bronchi most often found in bronchial asthma, chronic bronchitis, bronchiectasis, postoperative states, aspiration of foreign bodies, bronchial neoplasms (rarely)

  11. Compression atelectasis * Cause : the pleural cavity is partially or completely filled by fluid exudate, tumor, blood, or air (pneumothorax) mediastinum shifts away from the affected lung Contraction atelectasis * Cause : local or generalized fibrotic changes in the lung or pleura  prevent full expansion

  12. Resorption Compression Contraction

  13. Clinical Feature cough, but not prominent chest pain breathing difficulty low oxygen saturation pleural effusion (transudate type) cyanosis (late sign) increased heart rate

  14. Management • Based on the predetermined cause • Non Pharmacological non Invasive • chest physiotherapy : including postural drainage, chest wall percussion and vibration, and a forced expiration technique (called huffing) • Non Pharmacological invasive • Suctioning • Bronchoscopy • Pharmacological • Antibiotic if there is evident of infection • Nebulized bronchodilators and humidity may help liquefy secretions and promote their easy removal

  15. Learning Resources http://emedicine.medscape.com/article/296468-overview

  16. COPD

  17. COPD (chronic obstructive pulmonary disease ) * Emphysema (acinar level) * Chronic bronchitis (bronchial level) - Commonly caused by cigarette smoking - The fourth leading cause of morbidity and mortality in USA

  18. Emphysema : Condition of the lung characterized by irreversible enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis

  19. Types of Emphysema (according to its anatomic distribution within the lobule) Four major types : (1) Centriacinar(centrilobular) (2) Panacinar(panlobular) (3) Paraseptal(distal acinar) (4) Irregular * Centriacinar and panacinar cause clinically significant airflow obstruction * Centriacinar emphysema : > 95% of cases

  20. Centriacinar Emphysema The central or proximal parts of the acini, formed by respiratory bronchioles, are affected, whereas distal alveoli are spared - > severe in upper lobes, particularly apical segments - Walls of the emphysematous spaces : black pigment (++) - Inflammation around bronchi and bronchioles (+) - Severe  distal acinus may also be involved  differentiation from panacinar emphysema : difficult - >> in heavy smokers, often in association with chronic bronchitis

  21. Panacinar Emphysema Theacini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli - The prefix "pan" refers to the entire acinus but not to the entire lung - Tends to occur more commonly in the lower zones and in the anterior margins of the lung, and usually most severe at the bases. - Associated with α1-antitrypsin (α1-AT) deficiency

  22. Paraseptal Emphysema Theproximal portion of the acinus is normal, and the distal part is predominantly involved - More striking adjacent to the pleura, along the lobular connective tissue septa, and at the margins of the lobules - Occurs adjacent to areas of fibrosis, scarring, or atelectasis and is usually more severe in the upper half of the lungs - Multiple, continuous, enlarged airspaces from < 0.5 cm to > 2.0 cm in diameter, sometimes forming cystlike structures

  23. Irregular Emphysema (Airspace Enlargement with Fibrosis) The acinus is irregularly involved, almost invariably associated with scarring - In most instances, are asymptomatic and clinically insignificant

  24. Other forms of emphysema Compensatory Hyperinflation /Emphysema - Dilation of alveoli but not destruction of septal walls in response to loss of lung substance elsewhere Obstructive Overinflation - Caused by subtotal obstruction by a tumor or foreign object

  25. Bullous Emphysema - Large subpleural blebs or bullae ( Ø >1 cm ) - Occur in any form of emphysema - Occur near the apex, sometimes in relation to old tuberculous scarring. - Sometimes : rupture  pneumothorax Interstitial Emphysema * Entrance of air into connective tissue stroma of the lung, mediastinum, or subcutaneous tissue * Caused by : - alveolar tears in pulmonary emphysema - fractured rib that punctures the lung

  26. Possible Cause/Risk Factor Smoking Prolonged infection

  27. Pathogenesis # The protease-antiprotease imbalance hypothesis - Genetic deficiency of the antiprotease α1- antitrypsin (normally present in serum, tissue fluids, and macrophages, a major inhibitor of proteases particularly elastase) - Activated neutrophils (in smokers)  ROS  inactivation of α1-antitrypsin  elastase activity ↑  tissue damage  pulmonary emphysema

  28. # Smoking * Neutrophils and macrophages accumulate in alveoli - Chemoattractant effects of nicotine - Effects of ROS (free radicals) contained in smoke  activated neutrophils /macrophages  proteases (elastase, etc) release  tissue damage * Oxidant-antioxidant imbalance - Tobacco smoke : ROS/free radicals (++)  deplete antioxidant mechanisms  tissue damage * Activated neutrophils  ROS  inactivation of α1-antitrypsin

  29. Clinical course : Appear if > ⅓ of pulmonary parenchyma is damaged - Dyspnea - Cough - Wheezing confused with asthma - Weight loss - Barrel-chest - Expiratory airflow limitation  best measured through spirometry (the key to diagnosis)

  30. PULMONARY TB

  31. PULMONARY TUBERCULOSIS • Caused by : Mycobacterium Tuberculosis • Tissue reaction : - Granulomatous reaction (tubercle): - Hard tubercle - Soft tubercle • Mode of transmission : 1. airborne dropled 2. food 3. skin 4. feces

  32. Primary TBC * Develops in a previously unexposed, and therefore unsensitized person * Usually occur in children & infant * Sometimes occur in previously unexposed or profoundly immunosuppressedadults

  33. Pathogenesis : * Bacilli lower part of the upper lobe/upper part of the lower lobe (close to the pleura)  sensitization Ghon focus(1- 1.5 cm area of gray white inflammatory consolidation, caseous necrosis +)  regional nodes +, >>caseate (+)  Ghon complex(GF+ regional nodes) * In the first few weeks  lymphatic/ hematogenous spread may occur. * ± 95% of cases  cell-mediated immunity Ghon complex  fibrosis  calcification

  34. MACROS : The initial lesion : - Ø<2 cm, 1-2 cm of the apical pleura. - Sharply circumscribed, firm, gray-white to yellow - Central caseation, peripheral fibrosis - Fibrous encapsulation  fibrocalcific scars MICROS : -Coalescent tubercles with central caseation -Heal with fibrosis : spontaneously / tx (+) -Progress and extend along several different pathways

  35. PulmonaryTB

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