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  • Tujuan dari Respirasiadalah untuk menyediakan oksigen bagi seluruh jaringan tubuh dan membuang karbon dioksida ke atmosfer

  • Hidung

    Udara masuk disaring, dihangatkan dan dilembabkan oleh mukosa respirasi.Partikel kasar disaring oleh rambut hidung. halus: terjerat dalam lapisan mukus.Udara masuk faring: bebas debu, suhu sebanding suhu tubuh, kelembaban hampir 100 %

  • Rongga toraxParu adalah organ elastis terletak pada rongga dada/torax.Paru dilapisi oleh lapisan tipis kontinu yg mengandung kolagen & jar elastis yg disebut PLEURAPleura Parietalis melapisi rongga dada sedang Pleura viseralis melapisi paru .Rongga pleura: ruangan yg memisahkan pleura parietalis & viseralisCairan pleura: lapisan tipis antara pleura parietalis dg viseralis berfungsi memudahkan kedua permukaan tersebut bergerak selama pernapasan & untuk mencegah pemisahan torax & paru.Tekanan rongga pleura < tekanan atmosfer: untuk mencegah kolaps paru.

  • Rongga torax3 faktor yg mempertahankan tekanan negatif intrapleura normal:Jaringan elastis paru memberikan kekuatan kontinu yg cenderung menarik paru menjauh dr rangka torax.Kekuatan osmotik yg terdapat di seluruh membran pleura.Kekuatan pompa limfatik.Diafragma: otot berbentuk kubah yg membentuk dasar rongga torax & memisahkan rongga tersebut dari rongga abdomen.

  • Anatomi Saluran Pernapasan

  • Anatomi Saluran Pernapasan

  • AlveoliTerdapat 2 tipe sel alveolar:Pneumosit tipe I: lap tipis menyebar & menutupi > 90% daerah permukaan.Pneumosit tipe II: tanggung jawab pada sekresi surfaktan.Alveolus: suatu gelembung gas yang dikelilingi oleh jaringan kapiler batas antara cairan & gas membentuk tegangan muka yang cenderung mencegah pengembangan saat inspirasi & cenderung kolaps saat ekspirasi.Alveolus dilapisi zat lipoprotein (surfaktan) dapat mengurangi tengangan permukaan & resistensi saat inspirasi & mencegah kolaps alveolus (expirasi).

  • Bronchopulmonary segmentsLobulesAlveolar wall cell typesLUNGS 2terminal bronchiolerespiratory bronchiolepulmonary artery branchalveolar sac

  • AlveoliPembentukan & pengeluaran surfaktan oleh pneumosit tipe II disintesis secara cepat dari asam lemak yang diekstraksi dari darah, dg kecepatan pergantian yg cepat. Bila aliran darah ke paru terganggu (emboli) akibatnya jumlah surfaktan pada daerah tersebut berkurang.Produksi surfaktan dirangsang oleh ventilasi aktif, volume tidal yg memadai, hiperventilasi periodik (cepat & dalam) yg dicegah oleh kons O2 yang tinggi (inspirasi).Pemberian O2 kons tinggi jangka lama (pasien dg ventilasi mekanik) menurunkan produksi surfaktan & menyebabkan kolaps alveolar.

  • Pernafasan terdiri dari 4 proses :Ventilasi : Keluar masuknya udara karena adanya selisih tekanan yang terdapat antara atmosfer dan alveolusDistribusi : Pembagian udara ke cabang -cabang bronkhusTransportasi dan Difusi - Transport O2 dan CO2 dalam darah dan cairan tubuh ke dan dari sel - Difusi O2 dan CO2 antara darah dan alveoli Pertukaran gas-gas antara alveoli dan kapiler dipengaruhi oleh tekanan parsial O2 & CO2 dalam atmosferPerfusi : Aliran darah yang membawa O2 ke jaringan

  • JENIS RESPIRASI

  • RESPIRASI EXTERNAL

  • RESPIRASI INTERNAL

  • Active processBoyles LawINSPIRATIONPhrenic nerves (C3-5)Thoracic nerves (T1 T11)

  • Passive process at restEXPIRATIONinternal intercostals(11 pairs)external abdominal obliqueinternal abdominal obliquetransversus abdominisrectus abdominis760 mmHg762 mmHgelastic recoilsurface tension

  • Perubahan diafragma saat inspirasi & ekspirasi

  • Otot Pernapasan

  • Compliance is the ease with which the lungs and thoracic wall can be expanded during inspiration.COMPLIANCEelasticitysurface tensionRelated to two factors:destroys lung tissue (emphysema)fills lungs with fluid (pneumonia)produces surfactant deficiency (premature birth, near-drowning)interferes with lung expansion (pneumothorax)Compliance is decreased with any condition that:

  • PULMONARY VOLUMES, CAPACITIES, AND RATESSPIROGRAMIRVERVTVRVmaximum expirationVCTLC6000 ml5000 ml4000 ml3000 ml2000 ml1000 mlmaximum inspiration

  • Kontrol PernapasanOtot pernapasan diatur oleh neuron & reseptor pada pons & medula oblongata.

    Faktor utama pengaturan pernapasan: respon dari pusat kemoreseptor dalam pusat pernapasan terhadap tekanan persial CO2 dan pH darah arteri

  • Kontrol Pernapasan Persarafan parasimpatis/ kolinergik (mll nervus fagus) menyebabkan kontraksi otot polos bronkus shg menyebabkan bronkokonstriksi & peningkatan sekresi kel mukosa & sel goblet.

    Rangsangan simpatis ditimbulkan epinefrin mll reseptor adrenergik-beta2 menyebabkan relaksasi otot polos bronkus, bronkodilatasi, & berkurangnya sekresi bronkus.

    Sistem saraf nonkolinergik non adrenergik (NANC): melibatkan berbagai mediator seperti ATP, oksida nitrat, substance P, dan VIP (vasoactive intestinal peptide) respon penghambatan, meliputi bronkodilatasi, dan diduga berfungsi sebagai penyeimbang terhadap fungsi pemicuan oleh sistem kolinergik.

  • Kontrol Pernapasan

  • Signs and Symptoms of Pulmonary DiseaseDyspnea subjective sensation of uncomfortable breathing, feeling short of breathRanges from mild discomfort after exertion to extreme difficulty breathing at rest.Usually caused by diffuse and extensive rather than focal pulmonary disease.*

  • Derajat Dyspnea

    Tingkat Derajat Kriteria 0Normal Tidak ada kesulitan bernapss kecuali dengan aktivitas berat.1Ringan Terdapat kesulitan bernapas, napas pendek-pendek ketika terburu-buru atau ketika berjalan menuju puncak landai.2Sedang Berjalan lebih lambat daripada kebanyakan orang berusia sama karena sulit bernapas atau harus berhenti berjalan untuk bernapas.3Berat Berhenti berjalan setelah 90 meter untuk bernapas atau setelah berjalan beberapa menit.4Sangat beratTerlalu sulit bernapas bila meninggalkan rumah atau sulit bernapas ketika memakai baju atau membuka baju.

  • Dyspnea cont.Due to:Airway obstruction Greater force needed to provide adequate ventilationWheezing sound due to air being forced through airways narrowed due to constriction or fluid accumulationDecreased compliance of lung tissue*

  • Signs of dyspnea:Flaring nostrilsUse of accessory muscles in breathingRetraction (pulling back) of intercostal spaces*

  • BATUKBatuk merupakan gejala tersering penyakit pernapasanBatuk merupakan reflex pertahanan yang timbul akibat iritasi percabangan trakeobronkialBatuk yang berlangsung lebih dari 3 minggu harus diselidiki untuk memastikan penyebabnya.Bronkhitis kronik, asma, tubercolosis dan pneomonia merupakan penyakit yang secara tipikal memiliki batuk sebagai gejala yang mencolok

  • Cough may result from:Inflammation of lung tissueIncreased secretion in response to mucosal irritationInhalation of irritantsIntrinsic source of mucosal disruption such as tumor invasion of bronchial wallExcessive blood hydrostatic pressure in pulmonary capillariesPulmonary edema excess fluid passes into airways*

  • When cough can raise fluid into pharynx, the cough is described as a productive cough, and the fluid is sputum.Production of bloody sputum is called hemoptysisUsually involves only a small amount of blood lossNot threatening, but can indicate a serious pulmonary diseaseTuberculosis, lung abscess, cancer, pulmonary infarction.*

  • Cough that does not produce sputum is called a dry, nonproductive or hacking cough.Acute cough is one that resolves in 2-3 weeks from onset of illness or treatment of underlying condition.Us. caused by URT infections, allergic rhinitis, acute bronchitis, pneumonia, congestive heart failure, pulmonary embolus, or aspiration.*

  • A chronic cough is one that persists for more than 3 weeks.In nonsmokers, almost always due to postnasal drainage syndrome, asthma, or gastroesophageal reflux diseaseIn smokers, chronic bronchitis is the most common cause, although lung cancer should be considered.*

  • SPUTUM Pembentukan sputum: Orang dewasa normal mukus sekitar 100 ml dalam saluran napas tiap hari Mukus diangkut menuju faring dengan gerakan pembersihan silia yang melapisi saluran pernapasan bila mukus berlebihan proses pembersihan tidak efektif mukus tertimbun membran mukosa akan terangsang mukus dibatukkan keluar sebagai sputum.

  • SPUTUMSputum yang berwarna kekuning-kuningan menunjukkan infeksi.Sputum yang berwarna hijau merupakan petunjuk penimbunan nanah timbul karena adanya verdoperoksidase yang dihasilkan oleh polimorfonuklear (PMN).Sputum yang berwarna merah muda dan berbusa merupakan tanda edema paru akut.Sputum yang berlendir lekat dan warna abu-abu atau putih merupakan tanda bronkhitis kronik. Sedangkan sputum yang berbau busuk merupakan tanda abses paru atau bronkiektasis.

  • CyanosisWhen blood contains a large amount of unoxygenated hemoglobin, it has a dark red-blue color which gives skin a characteristic bluish appearance.Most cases arise as a result of peripheral vasoconstriction result is reduced blood flow, which allows hemoglobin to give up more of its oxygen to tissues- peripheral cyanosis.Best seen in nail bedsDue to cold environment, anxiety, etc.*

  • Central cyanosis can be due to :Abnormalities of the respiratory membraneMismatch between air flow and blood flowExpressed as a ratio of change in ventilation (V) to perfusion (Q) : V/Q ratioPulmonary thromboembolus - reduced blood flowAirway obstruction reduced ventilationIn persons with dark skin can be seen in the whites of the eyes and mucous membranes.*

  • Jari Tabuh Jari tabuh adalah perubahan bentuk normal falang distal dan kuku tangan dan kaki serta ditandai dengan Kehilangan sudut kuku yang normalnya 160 derajat. Rasa halus berongga pada dasar kuku.Ujung jari menjadi besar. jari tabuh berhubungan dengan peyakit paru (TB, abses paru, atau kanker paru). Penyakit kardiovaskuler (tetralogi fallot atau endokarditis infektif) atau penyakit hati kronik

  • Next2. Hipoksia (O2 yang tidak adekuat dalam tingkat jaringan) dan Hipoksemia (PaO2 dibawah normal normal 80-100 mmhg).Tanda dan gejala hipoksemia dan hipoksia tidak spesifik dan mencakup takipnea, dispnea, sakit kepala, pikiran yang bingung, takikardi, dan sianosis. 3. Hipokapnia dan hiperkapniaHipokapnia didefinisikan sebagai menurunnya PaCO2 45 mmhg. Penyebab langsung adalah selalu hipoventilasi alveolar (kegagalan dalam mengeliminasi CO2 secepat produksinya).

  • PainOriginates in pleurae, airways or chest wallInflammation of the parietal pleura causes sharp or stabbing pain when pleura stretches during inspirationUsually localized to an area of the chest wall, where a pleural friction rub can be heardLaughing or coughing makes pain worseCommon with pulmonary infarction due to embolism*

  • Inflammation of trachea or bronchi produce a central chest pain that is pronounced after coughingMust be differentiated from cardiac painHigh blood pressure in the pulmonary circulation can cause pain during exercise that often mistaken for cardiac pain (angina pectoris)*

  • Respiratory DisordersRespiratory disorder can be classified into different groupRespiratory tract infection Common cold,Influenza,Pneumonias,T.BDisorder of lung inflation Pleural pain and pleural effusionObstructive air way disorders Bronchial asthma, COPD, Emphysema, BronchitisPulmonary vascular disorderLung cancer

  • INFLUENZAPenyakit yang disebabkan oleh virus influenza. Gejala yang ditimbulkan antara lain pilek, hidung tersumbat, bersin- bersin, dan tenggorokan terasa gatal. Perlu diketahui virus ini selalu hanya bisa menembus saluran pernafasan atas saja , sehingga bisa disimpulkan saluran respirasi yang lebih dalam sangat resisten immun terhadap virus ini.

  • Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a roleIn susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning..

  • Causes and Triggers

    Allergies such as to pollens, mold spores, pet dander, and dust mites Infections (colds, viruses, flu, sinus infection) ExerciseAspirin or nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity, sulfite sensitivityUse of beta-adrenergic receptor blockers (including ophthalmic preparations)

  • Irritants such as strong odors from perfumes or cleaning solutions, air pollution, and tobacco smoke Weather (changes in temperature and/or humidity, cold air) Strong emotions such as anxiety, laughter, crying, and stressIndustrial triggers (wood, grain dust, cotton dust, isocyanate containing paints, aluminum, hair spray, penicillins)Beta blockers even in form of eye dropsCont

  • Gastroesophageal reflux diseaseChronic sinusitis or rhinitisOSA (obstructive sleep apnoe)ObesityAlergy bronchopulmonary aspergilosis COMORBID CONDITION

  • ASMAAsma ekstrinsik (alergik) (alergen, spt: debu,blu halus, serbuk) intrinsik (idiopatik)(fak nonspesifik spt flu, latihan fisik, emosi dapat memicu serangan asma) campuran(Komponen asma instrinsik+Ekstrinsik)

  • Two main pathophysiologic types of asthmaExtrinsic asthma; common in children, associated with a genetic predisposition and is precipitated by a known allergens. It is related to the formation of antibody IgE in the body

  • Immunological Mechanisms in Respiratory Diseases

  • Patofisiologi Asma

  • Intrinsic asthma; tend to develop in adulthood, and symptoms are triggered by non-allergic factors such as; Viral infection, irritants which cause epithelial damage and mucosal inflammationEmotional upset which mediates excess parasympathetic inputExercise which causes water ad heat loss from the airways

  • Pathophysiology

    Release of inflammatory mediator produce bronchial smooth muscle spasmVascular congestionIncrease vascular permeabilityEdema formationProduction of thick tenacious mucusImpair mucociliary functionThickening of air way wallIncrease response of bronchial smooth muscleDamage epithelium produce hyper responsiveness and obstruction

  • Faktor2 yang mengakibatkan obstruksi ekspirasi pada asma bronkial. A. Potongan melintang dari bronkiolus yang mengalami oklusi akibat spasme otot, mukosa yang membengkak, dan mukus dalam lumen, B . Potongan memanjang dari bronkiolusgambar

  • The mechanism of inflammation in asthma can beAcute; early recruitment of cells to the airwaysSubacute; resident and recruited cells are activated to cause a more persistent pattern of inflammation Chronic; cells damage is persistent and subject to ongoing repair, permanent change in the airway may occur with airway remodelling

  • Gambaran klinikBatuk yang memburuk pada malam hariSesak nafas Mengi atau Wheezing (a high-pitched whistling sound that occurs when exhaling) due to turbulent airflow through a narrowed airwaynafas pendek tersengal-sengal.Produksi sputum meningkat, sulit tidurHambatan pernafasanan reversibel Adanya peningkatan gejala pada saat olahraga, infeksi virus, eksposur terhadap alergen dan perubahan musim.Terbangun di malam hari krn gejala seperti di atas .

  • Investigations Pulmonary function testing (spirometry) Forced expiratory volume (FEV)Methacholine or histamine challenge testing Exercise testing Peak expiratory flow rate monitoring

  • Forced expiratory volume (FEV)Volume (litres)Time (second)1234Asthma patientNormal subjectFEV1FVC

  • Impairment

    ComponentofSeverityClassification of Asthma Severity (>12 yrs)IntermittentPersistentMildModerateSevereSymptoms2 d/wkbut not dailyDailyThroughout the dayNighttime awakening1x/wk but not nightlyOften 7x/wkSABA use2 d/wkbut not daily &not >1x on any dayDailySeveral times per dayInterference with activityNONEMinor limitationSome limitationExtremely limitedLung function Normal FEV1 between exacerbations FEV1: >80% predicted FEV1/FVC: normal FEV1 : >80% predicted FEV1/FVC: normal FEV1: >60% but

  • Leukotriene receptor antagonists Direct antagonist of mediators responsible for airway inflammation in asthmaBronchodilators Provide symptomatic relief of bronchospasm due to acute asthma exacerbation (short-acting agents) or long-term control of symptoms (long-acting agents)Drug categories Corticosteroids Highly potent agents that are the primary choice for treatment of chronic asthma and prevention of acute asthma exacerbations. Numerous inhaled corticosteroids are used for asthma and include beclomethasone (Beclovent, Vanceril), budesonide (Pulmicort Turbuhaler), flunisolide (AeroBid), fluticasone (Flovent), and triamcinolone (Azmacort).

  • 5-Lipoxygenase inhibitors Inhibit the formation of leukotrienes. Leukotrienes activate receptors that may be responsible for events leading to the pathophysiology of asthma, including airway edema, smooth muscle constriction, and altered cellular activity associated with inflammatory reactions Mast cell stabilizers Prevent the release of mediators from mast cells, which results in airway inflammation and bronchospasm. Indicated for maintenance therapy of mild-to-moderate asthma or prophylaxis for EIA

  • Three Steps of Asthma Treatment

    Step 1 - Control bronchospasm with short- acting b2 agonists or long-acting salmeterol

    Step 2 - Control inflammation with inhaled corticosteroids or leukotriene antagonist Step 3 - Control severe exacerbation with oral corticosteroids

  • Step 1 Is to control bronchospasm with inhaled b2 agonists. Short-acting b2agonists are appropriate for patients with mild, intermittent asthma who do not require daily maintenance therapy. Inhaled b2 agonists are effective, work quickly within 2 to 3 minutes and provide acute relief for up to 4 to 6 hours Remember that short-acting b2 agonists are indicated for use as rescue bronchodilators during acute attacks of bronchospasm.

  • When daily maintenance therapy is needed for more persistent symptoms, the long-acting b2 agonist salmeterol is an excellent and effective choice in treatmentSalmeterol can be taken once or twice a day as an inhaled bronchodilatorThe bronchodilating action of salmeterol is delayed in onset (20-30 minutes) but frequently lasts 8 to 12 hours when taken properly.

  • Step 2 Is to control inflammation when there is evidence of persistent or frequently recurring symptoms with inhaled corticosteroids or leukotriene antagonists, or the non-steroidal anti-inflammatory agents cromolyn sodium or nedocromil sodiumThis is maintenance anti-inflammatory therapy without any direct bronchodilator effect.

  • Inhaled corticosteroids and oral corticosteroids are used to control inflammation in asthma Corticosteroids prevent the migration of inflammatory cells and increase the responsiveness of airway b2 receptorsCorticosteroids have been shown to reduce acute bronchial hyperresponsiveness to irritants and may chronically blunt the early airway response to irritants with continued useThe new inhaled corticosteroid, fluticasone propionate, appears to possess a higher potency than other inhaled corticosteroids.Like other inhaled corticosteroids, fluticasone is indicated for the maintenance treatment of asthma as prophylactic therapy Recent studies have shown that it can reduce oral prednisone use while improving asthma control.

  • Inhaled nonsteroidal anti-inflammatory drugs like cromolyn or nedocromil may reduce symptoms in patients with mild to moderate asthmaThey are frequently prescribed in children and in adults with allergic asthmaThey inhibit the activation of mast cells and eosinophils, block inhaled neurogenic stimuli, and may reduce airway temperature changes that can trigger an asthma attackNedocromil may allow the reduction of corticosteroid use in selected patients

  • Step 3 Is to control severe exacerbations with systemic oral corticosteroids, i.e. prednisone 1 mg/kg or 40 to 60 mg daily for 1 to 2 weeksMany patients are steroid-dependent and frequently develop cushingnoid features such as hyperglycemia, fluid retention, weight gain with moon facies, and easy bruisability

  • Anticholingeric drugs like ipratropium may have an adjunctive role in asthma therapyThey block vagal pathways and produce bronchodilation by decreasing airway vagal toneThey are less potent than b2 agonists and have a slow onset of actionWhile they may reduce mucus secretion, there is no evidence that they modulate the inflammatory response

  • Oral theophylline and intravenous aminophylline were once the mainstay of asthma treatment, especially nocturnal asthmaOriginally thought to act as a phosphodiesterase inhibitor to increase cAMP, these methylxanthines are now though to antagonize adenosine, a mediator of acute inflammationTheophyllines reverse bronchospasm, enhance mucociliary clearance, and increase diaphragmatic contraction

  • However, theophylline is probably useful as an adjunct to b2 agonists and anti-inflammatory drugsAny benefit may be diminished somewhat by a narrow therapeutic range (5 to 15 g/ml) which can lead to serious and toxic consequences, e. g. seizures, tachyarrhythmias when exceeded

    Its use in the emergency treatment of asthma is not recommended but recent evidence suggest it may modulate chronic asthma symptoms more effectively than is generally perceived.

  • The use of cytotoxic agents, e. g. methotrexate, cyclosporine can not be recommended unless standard therapy with b2 agonists and anti-inflammatory drugs have failed

  • leukotriene receptor antagonists, Specifically, LTD4 receptor antagonist and 5-lipoxygenase inhibitors can completely block the acute phase response and block part of the delayed phase responseBlocking the generation of leukotrienes or blocking their actions on cells may be helpful in control of asthma and treatment of asthma attacks

  • DEFINISI PPOM/COPDPenyakit obstruksi saluran nafas kronis dan progresif yg ditandai oleh hambatan aliran udara yg bersifat non reversibel atau reversibel sebagian bersifat progresif & berhubungan dg respons inflamasi abnormal paru thd partikel atau gas beracun.

  • Bronkitis kronik& emfisemaMeskipun bronkitis kronik dan emfisema merupakan 2 proses yg berbeda, tp penyakit ini sering ditemukan bersama2 pada penderita COPD.Merupakan penyebab kematian terbanyakCOPD mnyerang pria 2x lebih banyak dari wanita karena faktor perokokFaktor etiologi utama adalah merokok dan polusi udara

  • FAKTOR RISIKO

    Host:

    - Genetik: Defisiensi alpha 1 anti tripsin atau antiprotease (menghambat aksi dari enzym protease)

    - Hipereaktivitas bronkusLingkungan:Asap rokok (faktor risiko utama - sigaret)Partikel debu & bahan kimia perindustrianPolusi udaraIndoor air pollution from heating and cooking with biomass in poorly ventilated dwellingsInfeksiStatus sosial

  • PATOGENESA

    Inflamasi /Keradangan kronis pd sal. napas, parenkim paru, sistem vaskuler paru pe makrofag, limfosit T (CD8+), netrofil release mediator LB4, IL8, TNFImbalance proteinase anti proteinaseStres oksidatifKetiga faktor diatas akan merusak struktur paru.

  • The theory of interplayis that this inflammatory process which includes alveolar macrophages in some way releases neutrophil chemotactic factors known as (IL-8 ) causing neutrophils to emigrate from the blood space into the airspace to release elastase .

    In normal circumstances alpha-1-antitrypsin binds to the elastase and prevents it from binding to elastin thus destroying the structure of the lungs.

  • Neutrophils

    in the blood and air space release more active oxygen species in smokers, than in non smokers, these together with the 1017 oxidants in inhaled cigarette smoke inactivate the alpha-1-antitrypsin at its active site. This reduces the ability of alpha-1-antitrypsin to bind to elastase by a factor of approximately 2000 allowing active ealstase to bind to elastin and cause the enlargement of the airspace that is seen in emphysema P-Selectin , L-seletin adhesions are important for the transport of inflammatory cells in the systemic circulation .

  • KLINIS

    Keluhan utama: sesak napas, batuk, dahak Sesak timbul progresif sp mengganggu aktivitas,men-dadak memberat bila tjd eksaserbasiBatuk kronis, memberat pagi hari, dahak mukoid purulen bila eksaserbasiSuara mengi (wheezing) Batuk darah blood-streaked purulen sputum (eksa-serbasi) Nyeri dada (pleuritis, pneumotoraks, emboli paru)Anoreksi & BB menurun progresif jelek

  • Noxious particles and gases

    Lung inflammation

    Host factors

    COPD pathology

    Proteinases

    Oxidative stress

    Anti-proteinases

    Anti-oxidants

    Repair mechanisms

  • PATOLOGI

    Saluran napas besar Hipertrofi kelenjar & pe jumlah sel Goblet hipersekresi mukus Saluran napas kecilRecycled injury & repair dinding sal. napas remodeling (pe kolagen & jar. ikat) penyempitan lumen & obstruksi sal. napas Parenkim paruDestruksi parenkim emfisema sentrilobuler Vaskuler pulmonal, Penebalan dd pembuluh darah

  • Pathophysiology

    The different pathogenic mechanisms produce the pathological changes which, in turn, give rise to the physiological abnormalities in COPD: mucous hypersecretion and ciliary dysfunction, airflow limitation and hyperinflation, gas exchange abnormalities, pulmonary hypertension, systemic effects.

  • Pathophysiology of COPD

  • According to GINAWhat is the difference between asthma and COPD (chronic obstructive lung disease)? COPD is a collective name for chronic bronchitis and emphysema, two diseases that are almost always caused by smoking. Many of the symptoms of COPD are similar to those of asthma (e.g. breathlessness, wheezing, production of too much mucus, coughing).

  • COPD/PPOM

  • BRONCHITIS KRONIS atau COPD type B

    Bronkitis kronik adalah inflamasi kronis saluran nafas yg ditandai dg udema dan hiperplasi kelenjar sub mucosal shg terjadi produksi mukus berlebihan ke batang bronchial akibatnya terjadi peningkatan resistensi sal pernafasaan secara kronik atau berulang dengan disertai batuk, yang terjadi hampir setiap hari selama sekurangnya tiga bulan dalam 1 tahun selama 2 tahun berturut turut. .

  • Etiologi Faktor lingkungan :- Merokok- Pekerjaan- Polusi udaraInfeksi berulang

    Faktor host :- usia- jenis kelamin- penyakit paru yangsudah ada

  • CHRONIC BRONCHITISChronic bronchitis is defined as "persistent cough with sputum production for at least 3 months in at least two consecutive years".

    The most important cause of chronic bronchitis is recurrent irritation of the bronchial mucosa by inhaled substances, as occurs in cigarette smokers.

    The pathological hallmarks of chronic bronchitis are congestion of the bronchial mucosa and a prominent increase in the number and size of the bronchial mucus glands. Copious mucus may be seen within airway lumens. The terminal airways are most susceptible to obstruction by mucus.

  • Pathophysiology of chronic bronchitis Irritants Hyperplasia and hypertrophy of mucous secreting cell Thick mucous Air trapping Sticky coating Air way obstruction Impaired ciliary function Edema Decrease mucous clearance Bronchial wall thickness and Lung defense system compromise inflammation Vulnerable for infection More infection more mucus

  • CHANGES IN LUNG VOLUMES

  • VENTILATION COSTIn COPD work of breathing is greater for any given level of ventilation than normal.VENTILATIONWORK OF BREATHINGNORMAL COPDSEVERE COPDMODERATE COPDThe cost of work at a given ventilation for normal and COPD patients (ACSM, 1998)

  • Damage to the epithelium impairs the mucociliary response that clears bacteria and mucus. Inflammation and secretions provide the obstructive component of chronic bronchitis.

    In contrast to emphysema, chronic bronchitis is associated with a relatively undamaged pulmonary capillary bed.

  • Emphysema or type A COPDDefinitionAbnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of the walls and without obvious fibrosisEmphysema is characterized by loss of elasticity of the lung and abnormal permanent enlargement of air spaces with destruction of the alveolar walls and capillary beds.

  • EtiologiEmphysemaSmoking the primary risk factorLong-term smoking is responsible for 80-90 % of cases.Prolonged exposures to harmful particles and gases from: passive smoke, Industrial smoke, Chemical gases, vapors, mists & fumesDusts from grains, minerals & other materialsAlpha 1-antitrypsin deficiency >>emphysemaGeneticsBronchitisAsthma

  • PathophysiologyExposure to inhaled noxious particles & gases inflammation imbalance of proteinases and anti-proteinases

    Dilatation & destruction + mucus secretion

  • FIG. 1. Inflammatory mechanisms in COPD. Cigarette smoke (and other irritants) activate macrophages in the respiratory tract that release neutrophil chemotactic factors, including IL-8 and LTB4. These cells then release proteases that break down connective tissue in the lung parenchyma, resulting in emphysema, and also stimulate mucus hypersecretion. These enzymes are normally counteracted by protease inhibitors, including 1-antitrypsin, SLPI, and TIMP. Cytotoxic T cells (CD8) may also be recruited and may be involved in alveolar wall destruction. Fibroblasts may be activated by growthfactors releases from macrophages and epithelial cells. CTG, connective tissue growth factor; COB, chronic obstructive bronchiolitis.

  • Pathophysiology

    Affects alveolar membraneDestruction of alveolar wallLoss of elastic recoilOver distended alveoli

    Over distended alveoliDamage to adjacent pulmonary capillaries h dead spaceImpaired passive expiration Impaired gas exchange

    Impaired gas exchange impaired expiration h CO2 HypercapniaRespiratory acidosis

    Damaged pulmonary capillary bed h pulmonary pressure h work load for right ventricle Right side heart failure (due to respiratory pressure) Cor Pulmonale

  • Gas Exchange is poor becauseLoss of alveolar structure base thereby causing decreased gas exchange surface areaMechanically, elastance is lost due to the constant stretching of distal airwaysConsequently, these patients are very compliant, because the natural tendency for the lung to collapse is inadvertently lost

  • This V/Q mismatch results in relatively limited blood flow through a fairly well oxygenated lung with normal blood gases and pressures in the lung, in contrast to the situation in blue bloaters. Because of low cardiac output, however, the rest of the body suffers from tissue hypoxia and pulmonary cachexia. Eventually, these patients develop muscle wasting and weight loss and are identified as "pink puffers."

  • *SYMPTOMScoughsputumdyspneaEXPOSURE TO RISKFACTORS tobaccooccupationindoor/outdoor pollutionSPIROMETRYDiagnosis of COPDGAS DARAH ARTERILABORATORY TESTCHEST X-RAY

  • Spirometry: Normal and COPD

  • 0

    5

    1

    4

    2

    3

    Liter

    1

    6

    5

    4

    3

    2

    FVC

    FVC

    FEV1

    FEV1

    Normal

    COPD

    3.900

    5.200

    2.350

    4.150

    Normal

    COPD

    FVC

    FEV1

    FVC

    FEV1/

    Seconds

  • Normally, the left side of the heart produces a higher level of blood pressure in order to pump blood to the body; the right side pumps blood through the lungs under much lower pressure. Any condition that leads to prolonged high blood pressure in the arteries or veins of the lungs (called pulmonary hypertension) will be poorly tolerated by the right ventricle of the heart. When this right ventricle fails or is unable toproperly pump against these abnormally high pressures, this is called cor pulmonale.

  • Prognosis ?

    Indikator: umur dan keparahan Jika ada hipoksia dan cor pulmonale prognosis jelekDyspnea, obstruksi berat saluran nafas, FEV1 < 0.75 L (20%) angka kematian meningkat, 50% pasien berisiko meninggal dalam waktu 5 tahun

  • Tujuan Terapi

    Memperbaiki keadaan obstruksi saluran nafasMencegah dan mengatasi eksaserbasi akutMenurunkan progresivitas penyakitMeningkatkan keadaan fisik dan psikis Menurunkan jumlah hari tidak masuk kerjaMenurunkan lama tinggal di RSMenurunkan angka kematian

  • NON FARMAKOLOGIMenghentikan kebiasaan merokokRehabilitasi paru-paru secara komprehensif dengan OR dan latihan pernafasanPerbaikan nutrisiTidak ada obat yang dapat menunda memburuknya fungsi paru jika pasien tetap merokok

  • Kortikosteroid benefit is very limited, laporan tentang efektivitasnya masih bervariasi, kecuali jika pasien juga memiliki riwayat asma Oksigen untuk pasien hipoksemia, cor pulmonale. Digunakan jika baseline PaO2 turun sampai < 55 mmHg Antibiotik digunakan bila ada tanda infeksi, bukan untuk maintenance therapy Vaksinasi direkomendasikan untuk high-risk patients: vaksin pneumococcus (tiap 5-10 th) dan vaksin influenza (tiap tahun) 1-proteinase inhibitor utk pasien yang defisiensi 1- antitripsin digunakan per minggu, masih mahal contoh: Prolastin

  • Tahap terapi pada PPOK yang stabil

    Tahap 1 : Ipratropium bromida (MDI) atau nebulizer, 2-6 puff 4 x sehari, tunjukkan cara penggunaan yang tepat, advis pasien ttg pentingnya penggunaan teratur dan efek samping yg mungkin timbul (mulut kering & rasa pahit), jika hasil trial : perbaikan FEV1 < 20% step 2Tahap 2 : Tambahkan -agonis MDI atau nebulizer, tunjukkan cara penggunaan yang tepat, advis pasien ttg pentingnya penggunaan teratur dan efek samping yg mungkin timbul (takikardi, tremor) jika tidak ada perkembangan: hentikan -agonis, jika ada perbaikan tapi kecil step 3

  • Tahap 3: Tambah teofilin,mulai dari 400 mg/hari dlm bentuk sustained released, sesuaikan dosis setiap interval 3 hari untuk menjaga serum level antara 10-15 g/ml, pantau ESO takikardi, tremor, nervous, efek GI; jika tidak ada perbaikan hentikan teofilin dan go to step 4Tahap 4: Coba dengan kortikosteroid : prednison 30-40 mg/hari selama 2-4 minggu, cek dengan spirometer (perbaikan 20%), titrasi dosis ke dosis efektif terkecil (< 10 g sehari), pertimbangkan penggunaan kortikosteroid inhalasi jika pasien tidak berespon baik kembali ke steroid oral

  • Terapi antibiotika

    Berdasarkan evidence terbaru yang tersedia, antibiotika harus diberikan pada pasien-pasien PPOK yang : Pasien dengan eksaserbasi akut dengan 3 tanda utama yaitu : increased dyspnea, increased sputum volume, increased sputum purulence (Evidence B), atau Pasien dengan eksaserbasi akut dengan 2 tanda utama, jika peningkatan purulensi sputum merupakan salah satunya (Evidence C) Pasien dengan eksaserbasi parah yang membutuhkan ventilasi mekanik, baik invasif maupun non-infvasif (Evidence B)

  • Key pointsPPOK adalah penyakit yang sebenarnya secara potensial dapat dicegah stop smokingSekali PPOK terjadi penderita akan memerlukan terapi yang kompleks yang efikasinya masih diperdebatkan para ahliPenyakit ini bersifat progresif dan ireversibel berbiaya besar baik baik personal maupun masyarakat

  • Difference between bronchitis and emphysema

    Productive coughbronchitis

    Classic signemphysema

    Late in common with infectionDyspneaLate in courseCommonWheezingIntermittentMildH/O smokingCommonCommonBarrel chestOccasionally classicProlonged expirationAlways presentAlways presentCyanosisCommonUncommonChronic hypoventilationCommon Late in coursePloycythemiaCommonLate in course

  • Bronchitis v. EmphysemaEasy to decompensateUsually relatively easy to treatCan cause emphysemaRarely are these patients ever having normal blood gasesUsually more difficult to decompensateDifficult to treatCan be caused by bronchitisEarly, blood gases are normal

  • Patofisiologi pneumotoraksAkibat peningkatan tekananIntrabronkial ( batuk/ bersin )Tekanan diteruskan s/d alveoli( locus minoris / Bullae - fibrotik pada alveoli )Alveoli robek sehinggamerobek pleura di sekitarnyaUdara masuk intrapleuraPneumotoraks

  • Berdasarkan penyebab terjadinyaPNEUMOTORAKS ARTIFISIALBedakan Tu-pleura dan Tu-paru ( dx )Proteksi Radioterapi Ca mamae ( tx )Haemoptisis Profuse ( tx ). PNEUMOTORAKS TRAUMATIKAkibat trauma pada dada. PNEUMOTORAKS SPONTANIatrogenik causa ??Penyakit kronis TB, COPD, Asma

  • Berdasarkan jenis fistelPNEUMOTORAKS TERBUKAP. Intrapleura = P. dunia luar ( two way )Tekanan ekspirasi + 2 = + 2Tekanan inspirasi 2 = - 2 PNEUMOTORAKS TERTUTUPP. Intrapleura P. dunia luar (no way )P awal + resorbsi paru P jadi paru belum ngembang sempurna.Tekanan ekspirasi 4 =- 4Tekanan inspirasi 12 = - 1

  • BERDASARKAN DERAJAT KOLAPS

    Pneumotoraks Totalis Pneumotoraks Partialis

    % Kolaps = ( A X B ) ( a X b ) X 100 % ( A X B )

  • Pneumotoraks parsial

  • Pneumotoraks total

  • Gejala KlinikSesak mendadak & memberat- Sesak tak di pengaruhi Posisi- Batuk- Dada terasa nyeri / kram / kemeng- Nampak sakit berat, keluar keringat dingin s/d syok- Napas tersengal sengal s/d sianosis

  • Penatalaksanaan PneumotoraksAntibiotika ~~ penyebab Anti Tuberkulosa ( OAT ) Anti Tusif ( codein ) Bronkhodilator Pencahar / Laxan Bed Rest / hindari kegiatan yang akibatkanpeningkatan tekanan intra pleura ( teriak, bersinkeras, mengejan dan batuk keras )

  • Komplikasi Pneumotoraks* Terjadi Infeksi Efusi Pleura ( Fluidopneumotoraks )Empyema ( Pyopneumotoraks ) Terjadi Trauma Hematotoraks Udara dari cav. Pleura meluasPneumomediastium Emfisema Cutis* Udara menekan ke organ sekitar Tamponade JantungGagal napas

  • Efusi Pleura

  • Efusi Pleura

    Adanya Cairan Pleura yang Volume nyalebih dari Normal ( Vol. normal: 1 20 cc )

  • Fisiologi cavum Pleura

  • Fisiologi Efusi PleuraVolume cairan pleura selalu konstan,akibat dari:# P. hidrostatik : 9 mmHg produksi oleh pleura parietalis# P. koloid osmotik : 10 mmHg absorbsi oleh pleura viseralis

  • Penyebab akumulasi cairan Pleura Tekanan koloid osmotik ( Hypolbuminemia ) Permeabilitas kapiler ( Radang, Neoplasma ) Tekanan hirostatik ( Gagal jantung ) Tekanan negatip intrapleura ( Atelektasis )

  • Pemeriksaan Fisik Efisi Pleura- Inspeksi nampak sakit, gerak dada sisi sakit tertinggal,nampak lebih cembung- Palpasi gerak dada sisi sakit tertinggal, Fremitus raba sisi sakit turun- Perkusi suara ketok sisi sakit redup pd.bag.bawah garis Ellis Damoiseau- Auskultasi suara napas sisi sakit turun /hilang

  • Sitologi cairan Pleura- Lekosit > 25.000 / mm3 Empyema- Netrophil > Pneumonia, TBC, Pancreatitis- Limphosit > TBC, limphoma, keganasan- Eosinophil > Emboli , Parasit, Jamur- Eritrosit 5 10 ribu/mm3 Pneumoni,Keganasan- Eritrosit 100 ribu / mm3 Keganasan, Trauma,Infark Paru- Sel ganas ditemukan pada 50 60 %Keganasan

  • Gambaran Radiologi Efusi Pleura< 300 CC : Secara fisik tak ada perubahan.Foto PA: sinus masih nampak lancip.Foto Lat: sinus nampak mulai tumpul> 500 cc : Gerak dada/ fremitus suara/fremitus raba menurun,suara ketok redup> 1000 cc: dada cembung, egofoni positip> 2000 cc: mediastinum terdorong

  • Foto ThoraxFoto Thoraks:Perselubungan Pada hemitoraksDextra dengan sinus frenicus costalis kanan tumpul

  • Penatalaksanaan Efusi Pleura- Evakuasi cairan pleura / torakosentesisvolume pengambilan maksimal 1000 ccsetiap kali pengambilan- Pemasangan WSD# Efusi Pleura massive# Efusi Pleura haemorhagic# Hematotoraks, Empyema# Chylotoraks, Chiliform

  • FARMAKOLOGIAntikolinergik inhalasi first line therapy, dosis harus cukup tinggi : 2 puff 4 6x/day; jika sulit, gunakan nebulizer 0.5 mg setiap 4-6 jam prn, exp: ipratropium or oxytropium bromide Simpatomimetik second line therapy : terbutalin, salbutamol Kombinasi antikolinergik dan simpatomimetik untuk meningkatkan efektifitas Metil ksantin banyak ADR, dipakai jika yang lain tidak mempan Mukolitik membantu pengenceran dahak, namun tidakmemperbaiki aliran udara masih kontroversi, apakah bermanfaat secara klinis atau tidak

    *********Immunological Mechanisms in Respiratory Disease

    Key Point: The mechanisms involved in the immune response have a role in the clinical effects seen in respiratory disease.

    Th2-cells by antigen-presenting cells. These Th2-cells then undergo selective expansion whichEventually results in the activation of B-cells andThe subsequent production of antigen-specific IgEUpon re-exposure to the same allergen an acute response is elicited that is triggered through cross linking of IgE antibody-loaded high-affinity IgE receptors on mast cells and basophils*