You are on page 1of 85

PPOK (Penyakit Paru Obstruksi Kronis

)

Definisi
• GOLD (Global Initiative for chronic obstructive lung disease): COPD adalah suatu penyakit yang ditandai dengan adanya hambatan aliran napas

yang tidak sepenuhnya refersibel. Hambatan
saluran napas tersebut biasanya bersifat progresif dan berhubungan dengan respon inflamasi abnormal paru terhadap partikel atau gas iritan.

Penyebab pembatasan saluran napas COPD
• Irreversible:

-fibrosis dan penyempitan saluran napas
-hilangnya elastisitas oleh karena alfeoli telah rusak

• Reversible
-akumulasi sel-sel inflamasi, mukus, plasma bronkus -kontraksi otot polos sentral maupun perifer -hiperinflasi dinamis selama exercise eksudat pada

Faktor Resiko
1. • • • 2. • • • • Host Faktor Genes (alpha1-antitrypsin deficiency) Hyperesponsive Lung growth (prematur) Exposure Asap rokok (90%) Debu dan zat kimia di tempat kerja Infeksi (streptokokus, S. pneumonia, H. influenza) Status sosioekonomi

Bronchitis cronis dan emphisema . Emphisema • 3.Yang termasuk dalam COPD • 1. Bronchitis cronis • 2.

tidak disebabkan penyakit lainnya. sekurang-kurangnya 2 tahun berturut-turut.Bronchitis Cronis • Keadaan dengan produksi mukus trakeobronkial yang berlebihan sehingga menimbulkan batuk kronis berdahak minimal 3 bulan dalam setahun. . • Obstruksi saluran napas adalah persistent dan irreversibel.

.etiology • • • • • Penyebab utama bronkitis kronis adalah asap rokok (90% kasus). faktor genetik. inhalation chemical irritants. infeksi saluran napas yang berulang.

Wheezing 5. Dyspneu pada saat aktivitas 4. Batuk dan sputum meningkat pada pagi hari 3. Tahap akhir: cor pulmonal/heart fail • edema peripheral • Distensi vena leher .Tanda dan gejala 1. Tanda utama bronkitis chronik adalah batuk persisten dengan produktif sputum 2.

increase mucus production .Pathogenesis • Faktor inisiasi (asap rokok 90%) Kerusakan bronkus. increase bronchial wall thickness. increase cilliary dysfunction Chronic bronchitis . hyperplasi bronchial mucus gland and goblet cell. Fibrosis mucous membrane. bronkiolus Continued and repeat injury (smoking) Continued and repeated infection Chronic inflamasi. bronkiolus Hipersekresi mukus bronkospasme infeksi Obstruksi reversibel pada bronkus.

.

Onset symptom 4. History 1. purulen : chronic.diagnosis A. Dyspneu . Cough : smoker : overweight : after age 40 yr : excessive. Lifestyle 2. Sputum 5. Weight 3. more severe in morning : mild to moderate 6.

4. 3. 7. 6. Keluhan pasien 1. 5. 2. Batuk kronis dengan seputum mukopurulen Malaise Nyeri otot Fatigue Insomnia Loss of libido Dyspneu (mild-moderate) .B.

C. depend on the severity of disease 6. Percusion : normal 7. 5. Edema : present Cyanosis : present in advanced disease Use of accesory muscle to breath: absent until end stage Antero posterior chest diameter : normal Auscultation of chest : wheezing. 4. crackles. Tanda fisik 1. Other : evidence of right-sided heart failure ( cor pulmonal) . 2. 3. ronchi. Jugular vein distention : present 8.

D. Chest radiografi: increase bronchial vasculer marking. Hematocrit: polycitemia . General diagnosis test 1. increase Pa CO2) 3. Artery blood gas analisys: decrease PaO2 ( <65 mm HG. right ventriculer hipertrofi. enlarge horizontal heart 2. atrial arytmia 4. ECG : Right axis deviation.

Radiology Pasien .

Pulmonary finction test • Residual folume : increase • Total lung capacity : normal • Forced expiratory volume: decrease • Vital capacity : normal or slight decrease .E.

Produce pulmonary hypertension Right ventricular end diastolic pressure increase Leading to right ventricular dilation and right sided heart failure .right-sided heart failure ( cor pulmonal) Cronic broncitis Small pulmonary artery related to inflammation in the bronchial wall and the compensatory spasm of pulmonary blood vessel from hipoxia.

.

Manifestasi klinik • Terjadi kelebihan cairan tubuh (edema) • Jugular vena distensi • Cyanosis ( stadium akhir) .

.

.

tanpa adanya fibrosis .Emphisema • Emphisema adalah kelainan pada paru yang ditandai dengan pembesaran abnormal yang permanen pada rongga udara distal bronkial terminal. disertai dengan kerusakan dinding alveolus .

Etiology  Cigarette smoking (>70 pack-year)  Air polution  Occupation ( working with or near asbeston)  A1-antytripsin .

dan sering terjadi pada seseorang dg usia >50 th • Merokok dg jumlah >70 bungkus / tahun merupakan faktor resiko tinggi terjadi PPOK .• Emphisema cenderung berkembang dalam waktu yang lama.

. mulai sekitar usia 30. and decrease bronchial muscle . mencerminkan perubahan serupa dengan yang terlihat pada emfisema :  Loss of alveoli  Increase in the size of alveolar duct  Loss of gas exchanging surface area (4% per decade).• proses penuaan normal.

atau usia <50 th pada perokok Deficiency A1-antitrypsin Penyakit herediter yang ditandai dengan penurunan jumlah A1 antitrypsin pada serum (2550 mg/dl) <2% pasien emphisema .• Ketika emphisema terjadi pada usia mudadewasa.

macrofagh ). .• A1-antitrypsin adalah suatu enzim yang berfungsi sebagai pelindung jaringan alveolus dari kerusakan yang disebabkan oleh zat proteolisis (protease) dari ( neutrophil.

Paraseptal emphisema ( dilatasi distal acinus) 4. Panacinar (Panlobuler) emphisema • Dilatasi pada bagian peripheral ( duktus alveolus dan alveolus) • Berhubungan dengan A1 antitripsin deficiency 3. Irreguler emphisema (irreguler pd acinus karena terbentuk scar) .Type emphisema 1. Centriacinar ( centrilobuler emphisema) • Dilatasi pada respiratory bronkhiolus • Terjadi pada perokok berat dan berhubungan dengan bronkitis kronis 2.

.

Panacinar emphisema Centriasinar emphisema .

patogenesis .

•Destruction of alveolar tissue and septa •Increased mucus secretion •Inflammation in the bronchiolus •Impaired in air way clearence •Loss of radial traction with collapse of bronchial leading to air trapping .

3.Manifestasi klinis 1. 2. 6. 4. 5. 7. Dyspneu is usually the first symptom Weight loss Barrel chest Prolong expiration Sits forward in a hunched-over position Breathes trough purs lips Pink puffer .

Pink puffer .

Barrel chest .

diagnosis A. Lifestyle : smoker 2.History 1. Onset symptom : after age 50 yr 4. Cough : minimal or absent 6. Weight : weight loss 3. Dyspneu : progresif exertion dyspneu . mucoid 5. Sputum : mild.

Patient complain
• Dyspneu on exertion, • fatigue (kelelahan) , • insomnia

C. Tanda fisik
1. Edema 2. Cyanosis : absent : absent

3. Use of accesory muscle to breath: present
4. Antero posterior chest diameter : barrel chest

5. Auscultation of chest
heart sound, prolong expiration

: decrease breath sound,

6. Percusion
7. Jugular vein distention 8. Other

: hyperersonance
: absent : purs lips breathing

D. General diagnosis test
1. Chest radiografi: hyperinflation, flat, low diafragma, normal or small vertical heart 2. Artery blood gas analisys: decrease PaO2 ( 60-80 mm HG), normal or increase Pa CO2 (increase with advancing disease) 3. ECG : normal or tall symmetrical P wave, tachycardi if hypocix 4. Hematocrit: normal

Pulmonary finction test • Residual folume : increase • Total lung capacity : increase • Forced expiratory volume: decrease • Vital capacity : decrease .E.

polusi Normal spirometry: FEV1/FVC pasca bronchodilator >70% FEV1 ≥80% . sputum/dyspneu Exsposure to risk factor: merokok.Derajat PPOK 1. • • • Pasien beresiko chronic symptom : batuk.

2. PPOK RINGAN • FEV1/FVC < 70% • FEV1 ≥80% • WITH OR WITHOUT SYMPTOMS 3. PPOK SEDANG • FEV1/FVC < 70% • 50%≤FEV1<80% • WITH OR WITHOUT SYMPTOMS .

PPOK BERAT • FEV1/FVC < 70% • 30%≤FEV1<50% • WITH OR WITHOUT SYMPTOMS 5. PPOK SANGAT BERAT • FEV1/FVC < 70% • FEV1<30% OR FEV1<50% • Predicted plus chronic respiratory failure .4.

Tuberculosis 4. CHF (Congestive Heart Failure ) . Asma bronchial 2. Bronkiektasis 3.DIAGNOSA BANDING 1.

Asma bronchial • Adalah penyakit inflamasi kronis pada saluran nafas yang menyebabkan gejala berulang yi: wheezing.1. sesak nafas. dada terasa sesak. dan batuk. atau pada pagi hari. terutama pada malam hari. .

• Gejala tersebut berhubungan dan airflow nafas) yg dengan limitation bersifat bronchokontriksi (pembatasan saluran reversibel (spontan atau dg treatment) .

Atopic asthma  Begin in childhood  A positive family history  Asthmatic attack are often preceded by allergy rinitis. . food.Type asthma 1. pollen. urticaria  Trigger by environmental antigent : dust.

allergen macrophage CD4 sell TH2 cell pathogenesis B sell eosinophil IGE mediator Mast sell mediator neutrophil Monosit Limphosit Basofil Bronchospasme Increase vascular permiability Mucus production Immediate phase (minutes) Damage ephitelium Late phase ( 4-8 hours) .

bacteri.2. parainfluenza Virus).  A positive family history is uncommon  Serum IGE normal  No other associated allergies  Skin test are negative . Nonatopic asthma  Trigger by respiratory tract infection  Virus ( Rhinovirus.

leukotrinbronchokontriksi . drug induce asthma aspirin-inhibiting COX pathway of asam arachidonat-without affecting lipoxygenase route.• 3.

tachypneu dada terasa sesak. sticky/lengket) • ( beberapa pasien dg batuk kering dan yg lainnya dg batuk produktif.Tanda Klinis • • • • sesak nafas. scant/sedikit.)  serangan asthma berlangsung hingga beberapa jam dan diikuti oleh batuk yang berkepanjangan. tachicardi. . Batuk dan peningkatan sputum ( thick/kental. wheezing.

Pemeriksaan sputum • Charcot-leyden cristal (eosinophil membrane). tacipneu.diagnosis 1. 5. 3. eosinophil. 2. Spirometri • Airflow obstruction is indicate by FEV1/FVC <75% 4. Pemeriksaan darah: peningkatan sell darah putih. batuk. Pemeriksaan fisik • Sesak napas. Radiographi • Normal atau hyperinflasi dg diafragma mendatar pada progresif disease. wheezing. . tachicardi. eosinophil.

Bronchi pd anak anak sangat mudah mengalami kerusakan : overinflasi dan distensi karena inflamasi dan inveksi .Bronchiektasis Bronkiektasis adalah dilatasi dari bronchi Anak anak mempunyai resiko tinggi bronchiktasis karena faktor anatomi saluran nafas: small (kecil). soft (lunak. elastic bronchi.lemah).

pembentukan pus.patogenesis  Inflamasi dan infeksi berulang ( H.  Menyebabkan obstruksi saluran nafas . squamous cell metaplasia. Influenza)  Inflamasi menyebabkan kerusakan dinding central bronchi dan perifer bronchi dan bronchiolus = persistent dilation of the medium-size bronchi and bronchiolus  Kerusakan ephitel cillia.

Green or yellow sputum 5. skin pallor. . Chronic productive cough 2. Other clinic feature: hemoptysis.Manifestasi klinik • Child ussualy present: 1. bad breath. Copious amount of purulent 3. Foul-smelling 4. ronchi.

purulen sputum 3. Radiografi: increase bronchial marking. hypercapnea (increase PaCO2).Diagnosis 1. History of chronic productive cough 2. thickening of bronchial walls 4. Produce copious amounts of foul-smelling. Arteri blood gas: hypoxemia (decrease PaO2). . Pulmonary function test: decrease airflow and vital capacyti in advanced cases 5.

CHF dibagi 2:  Left-sided heart failure  Rigth-sided heart failure .CHF (Congestive Heart Failure )  Penyebab utama CHF adalah ischemic cardiomiopathy dan hypertensi  Manifestasi klinis.

Systemic hypertension . Left ventrikel infarction 2.Left-sided heart failure Disebabkan oleh: 1. Aortic 4. Cardiomiopaty 3.

patofisiology Left Ventricular Failure Backward effect Decrease ejection fraction Increase left ventricel preload Increasi left atrium pressure Increase pulmonary pressure Decrease tissue perfusion Forward effect Decrease cardiac output RAS activation Fluid retention Increase right ventriculer after load Pulmonary congestion Right ventricular hypertrophi .

Dyspneu on exertion 2. Confusion 6. anxiety . Increase heart rate 4.Cough 4.Backward effect 1. Restlessness (gelisah) 5. Fatigue (kelelahan) 2.Basilar crackles Forward effect 1.Orthopneu 3. Oliguria 3.Cyanosis 6.Paroxysmal nocturnal dyspneu 5.

Semua penyebab gagal ventrikel kiri . Infark ventrikel kanan 2. Penyakit paru 3.Right ventricular failure • Penyebab: 1.

Patogenesis Right Ventricular Failure Backward effect Decrease ejection fraction Increase right ventricel preload Increasi right atrium pressure Sistemic congestion Forward effect Decrease output to left ventricle Decrease left ventricle Cardiac output RAS actifation Fluid retention Decrease tissue perfusion hepar splen gastroin testinal Ren Lower extremitas .

Increase heart rate 4. Fatigue 2.Ascites 3. Confusion 6.Hepatomegali 2.Vena jugular distensi Forward effect 1.Anorexia 5. anxiety .Subcutan edema 6. Restlessness (gelisah) 5.Splenomegali 4.Backward effect 1. Oliguria 3.

bicara. . bersin. bentuk batang. • Cara penularan : Kuman masuk secara inhalasi (<5mikrometer) pada saat pasien batuk.TBC (Tuberculosis) • Kuman penyebab : mycobakterium tb (bakteri aerob. tahan asam).

TBC ( arabinomanan) Menghambat aktifasi macrofagh Multiplikasi M.Tuberculosis Jaringan Paru Fagosit alveolar macrofagh dindingM.pathogenesis M.TBC dimacrofagh Ghon tubercle Sel T CD4 TNF Melisiskan sel terinfeksi Peningkatan macrofagh .

BB turun.Manifestasi klinis  Batuk kronis >14-21 hari ( batuk kering.batuk darah )  demam subfebris (demam influenza)  Berkeringat pada malam hari  malaise (anoreksia. sakit kepala.berminggu minggu/ berbulan bulan Purulent sputum. nyeri otot)  Sesak nafas ( penyakit yg sudah lanjut) .

TB Suspects Sputum AFB Microscopy Two or three smears + Only one smear + Three smears - Non anti TB antibiotic X-ray and medical officer’s judgment Repeat AFB No improve improve One or more smears + All smears - X-ray and medical officer’s judgment No TB YES TB .

Management of COPD 1. Farmakology A. pulmonary rehabilitation. methylxanthin B. Bronchodilator anticholinergic. Non-farmacology Reducing risk factors.β2-adrenergic reseptor agonist. oxygen terapy. Cortichosteroid C. 3. Surgical therapy . Antibiotic 2.

Inhaled Anticholinergics  Effect: decrease bronchoconstriction and glandular mucus  Short-acting inhaled anticholinergic -such as : ipratropium -maximum bronchodilation in 1-2H. maintained approximately 4H  Long-acting inhaled anticholinergic -such as: tiotropium -result in prolonged bronchodilation for 24H or more -dose: once-daily dosing regiment .Bronchodilator A.

• Available as metered-dose inhalers. POSSIBLESIDEEFFECTS • Coughing • Dry mouth • Nausea • Headache Anticholinergics – Short-Acting and Long-Acting .COMBIVENT® GENERIC Ipratropium Ipratropium and Albuterol Ipratropium • Open airways by relaxing tight muscles around them. • Always inhaled. dry powder inhaler. or as a liquid for nebulization. • Most often used together with short-acting or long-acting beta2-agonists.

Inhal β2-adrenergic reseptor agonist  Effect : induce bronchodilation  Short-acting B2-adrenergic receptor agonis SABAs -such as: terbutalin&albuterol -as needed basis to relieve symptoms because a rapid onset of action.B. -provide effect bronchodilation 4-6H .

• Available as metered-dose inhaler. • Usually inhaled. although occasionally taken as tablets. POSSIBLESIDEEFFECTS • Rapid heartbeat • Nervousness • Tremors and shakiness • Nausea • Dry mouth and throat • Increased blood pressure • Muscle weakness • Decreased blood potassium level Beta2-Agonists – Short-Acting .Albuterol Albuterol and Ipratropium Open airways by relaxing tight muscles around them. • Carry the inhaler with you wherever you go for quick relief from sudden shortness of breath. dry powder inhaler. or as a liquid for nebulization.

formoterol and salmeterol . Long-acting β2-adrenergic receptor agonists (LABAs) .maintenance therapies for the long-term prevention and reduction of COPD-related symptoms -effect >12H .

Salmeterol Formoterol Open airways by relaxing tight muscles around them. • Not to be used for quick relief of shortness of breath. • Often dry powdered inhalers. • The inhaled medicines are only taken twice a day. POSSIBLESIDEEFFECTS (Very uncommon) • Racing heart • Tremors (shaking) • Nervousness (gelisah) LONG-ACTING BETA2 AGONISTS . although they are occasionally taken as tablets.

 such as : aminophylline and theophylline  use of these agents is considered controversial because: third-line treatment option after inhaled β2-agonists and anticholinergic agents because wide range of dose-related toxic effect & its limited clinical efficacy. headaches. nausea and heartburn.C.  theophylline continues to be used in the treatment of COPD primarily because of its low cost . Methylxanthines. insomnia.  Adverse events associated with methylxanthine treatment include possible fatal atrial and ventricular arrhythmias. convulsions.

 Results of a study conducted by van Noord et al.demonstrated that combination therapy with formoterol plus tiotropium improved pulmonary function.Bronchodilator Combination Therapy  Combined treatment with a β2-adrenergic receptor agonist. as assessed by several lung function parameters (e.g. . and/or theophylline have been shown to provide additional improvements in lung function and health status compared with single-agent therapy for COPD. an anticholinergic agent. FVC and FEV1). more than improvements achieved with either component alone.

. • The 2006 GOLD guidelines recommend ICS therapy with agents such as beclomethasone dipropionate. budesonide.Stage III to stage IV COPD • Oral corticosteroids (OCS) and ICS are used as add-on therapy in very specific situations in the management of stable COPD. fluticasone propionate. mometasone furoate and triamcinolone acetonide for the treatment of patients with advanced COPD (FEV1<50% predicted) who experience repeated exacerbations.

PULMICORT budesonid® Fluticasone Beclomethasone Reduce inflammation and swelling of the airways. not your entire body. they generally only affect your lung and airways. Inhaled Steroids . • Because they are inhaled.

• Pneumococcal vaccine is also recommended for patients >65years old = to reduce pneumococcal pneumonia in patients with COPD .influenza vaccination • The influenza vaccine has been shown to reduce serious illness for patients with COPD by as much as 50%.

nutritional counselling. Pulmonary Rehabilitation • • exercise training.Non-pharmacologic Therapy for COPD A. Reducing Risk Factors • • • Smoking cessation Reducing and eliminating occupational exposures to airborne pollutants Consistent and persistent patient education and counselling B. and patient education Exercise training should include aerobic and resistance exercises to improve aerobic capacity and muscle strength .

Lung transplantation .Oxygen Therapy • Oxygen therapy decrease pulmonary hypertension. • Surgical Options • Lung volume reduction surgery (LVRS). improves the mental and emotional states of patients. increases exercise capacity and lung function.

.

tightness in the chest. • associated with infections (S.Pneumonia. increased cough sputum production.Managing COPD Exacerbations • Patients who experience acute exacerbations commonly present with increased breathlessness. and fever. change in colour and tenacity of sputum. .influenza) of the tracheobronchial tree and with air pollution. H. wheezing.