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A 52-year old man present to your office for an accute visit because of coughing and shortness of breath. He is well-known to because of multiple office visit in the past few years for similar reason. He has chronic smokers caugh,but reports in the past 2 days his cough has increased,his sputum has changed from white to green in color and he has had to increase the frequency with which he uses his albuterol inhaler. He denies having fever, chest pain, peripheral edema, or other symptoms. His medical history is significant for hypertensio, pheripheral vascular disease, and 2 hospitalization pneumonia in the past 5 years. He has a 60-pack-history of smoking and continuous to smoke 2 packs of cigarettes a day.
On examination, he is in moderate respiratory distress. His temperature is 98.4F degree, his blood pressure is 152/95 mm Hg, his pulse is 98 beats/min, his repiratory rate is 24 breaths/min, and he has an oxygen saturation of 94% on room air. His lung is significant for diffuse expiratory wheezing and a prolonged expiratory phase of respiration. There are no sign of cyanosis. The remindeer of his examination is normal. Chest x-ray done in your office shows an increased anteroposterior (AP) diameter and flattened diaphragms, otherwise clear lung fields.
introduction
In this time,there are a lot of problem about pulmonary dissease which increased the precentage of mortality. In this case we will talk about the obstruction of respiratory way. Respiratory way can sufferer of an acute obstruction which is happen in superior of respiratory way (supraglotic), middle of respiratory way (intraglotic),or under of respiratory way(infraglotic). If the obstruction happen in the under of the respiratory way so it maybe cause by an asthma or COPD. Yeah we will concern about the COPD it self
In the past few years chronic obstructive pulmonary disease(COPD) or sometimes we call PPOK in bahasa is an interesting topic in this world, because there are an increases of precentage of mortality cause by COPD. As cause of the death COPD has stay as the fourth grade after the heart attack and cerebrovascular disease.
Main idea
What is COPD mean? COPD is a chronic obstructive pulmonary disease that marked by the blocked of respiratory way that not reversible at all. This inhibitation of the respiratory way is always progressive and related to the lungs inflamation cause by particle, or even dangerous gas.
DEFINITION
COPD
AIRFLOW LIMITATION IN SMALL AIRWAYS PROGRESSIVE
CHRONIC INFLAMMATIO N
PARTIAL REVERSIBLE
IRREVERSIBLE
2 EMPHYSEMATOUS LUNG
GOLD [ NHLBI WHO ] GUIDELINES MANAGEMENT STRATEGY OF COPD WHO 2020 MORTALITY 3 million/year
HOSPITAL MORTALITY 10 %
INCREASE OF 51 % ACUTE EXACERBATION IN HOSPITAL ADMISSION BETWEEN 1991 - 2000 PREMATURE DEATH
Trigger factors: -smoke of ciggarete An active smoker A passive smoker -air polution Indoor polution Smoke of stove Outdoor polution smoke of vehicle Iritation particle, chemicle stuff, dangerous gasoline. -infection of under of respiratory way
PHATOGENESIS OF EMPHYSEMA
DIAGNOSIS OF COPD
1
SYMPTOMS COUGH SPUTUM DYSPNEA
2
EXPOSURE TO RISK FACTORS Tobacco Smoke Occupation Indoor / outdoor pollution
SPIROMETRY
How to diagnose?
Taking a history Anamnesis Trigger factors Medical history PPOK in his family? A hospitalized in past time? The effect of this disease to his activity
Physical examination
pursed lips breathing Takipneu emfisematous chest or barrel chest Physical appearance pink puffer or blue bloater Flattened of sela iga Hiperthropy of otot bantu nafas Bunyi nafas vesikuler melemah Prolonged expiratory wheezing
Ro. Thorax
What intervention woud be most helpful to reduce the risk of future exacerbation of this condition ?
COPD MANAGEMENT
1
ESTABLISH DIAGNOSIS ASSESS SYMPTOMS STOP SMOKING HEALTHY LIFESTYLE IMMUNISATION
2
TREAT OBSTRUCTION BRONCHODILATORS
3
ASSESS FOR HYPOXIA LONG TERM OXYGEN THERAPY
1 STOP SMOKING
TRIAL OF BUPROPION NICOTINE REPLACEMENT
COPD PHARMACOTHERAPY
2 4
INHALED CORTICOSTEROIDS ONLY FOR CONCOMITANT ASTHMA
BRONCHODILATORS
MUCOLYTIC S 1
ANTIOXIDANTS 2
N-ACETYLCYSTEINE
step 3: adding teofilin, start from 400 mg/day check ESO takikardi , tremor, nervous, efek GI; if there are no progression stop teofilin dan go to step 4 Tahap 4: try kortikosteroid : prednison 30-40 mg/hari for 2-4 minggu, chcek spirometery (progression 20%),titrasi doxe to doze smaller efectivity(< 10 g sehari), if there are no progreesion kembali ke steroid oral
NEW BRONCHODILATORS
2 MEDIATOR ANTAGONISTS 3 PROTEASE INHIBITORS
TRIOTROPIUM
pharmacology
Antikolinergik 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
mempan
Mukolitik membantu pengenceran dahak, namun tidak
memperbaiki aliran udara masih kontroversi, apakah bermanfaat secara klinis atau tidak. 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
infeksi, bukan untuk maintenance therapy Vaksinasi direkomendasikan untuk highrisk patients: vaksin pneumococcus (tiap 5-10 th) dan vaksin influenza (tiap tahun) 1-proteinase inhibitor utk pasien yang defisiensi 1antitripsin digunakan per minggu, masih mahal contoh: Prolastin
prognose
Depends on age and the progresivity of this illness if there are hipoksia and cor pulmonale bad prognosis Dyspneu, bad obstruction of respiratory way 50% patient has risk of death in 5 years.
conclusion
COPD is a disease that can be prevent potentialy stop smoking If COPD happened in once time patient need the complicated therapy. This disease is progressive and ireversible need an expensive price for a personal or public it self.
Any question?