TITTLE CASE : COPD

Group Puskesmas (Puskesmas Mergangsan) Participants : dr. Yulaika Kusuma Wardani dr.Tri Wahyuliati, SpS,M.Kes. dr.Siti Kusdinariyalun H. dr. Pramudi Darmawan W., M.Kes dr. Sandra Kartika Consultant : dr. Sumardi, SpPD-KP

I. CASE A. Patients Identity

Name Sex Age Height Weight Marital status Occupation Address Examination date : : : : : : : : : Mr. SS Male 81 years old 159 cm 42 kg widower toys vendor (in the past) Dalem, Rt 42 Rw 10 Purbayan Kotagede 9 July 2010

B. Anamnesis 1. Chief complaint 2. Current History

3. Past History

: Dyspnoe : Patient came to primary health care with dyspnoe complaint along with cough for 3 days. Dyspnoe often recurrent if he gets cool weather, exhausted, and inhales smoke. Cough with white yellowish sputum occurred, often slimy purulent. Patient complaints if he cant relieved in breathing. : Since 1964 patient has often experienced dyspnoe and diagnosed as suffered from asthma. In 2006, patient ever had outpatient treatment in BP Paru with persistent dyspnoe and cough (more than 3 months). At that time, pulmonary x-ray result showed Chronical Bronchitis. The patient smoked at the age of 16-56 years old. He usually smoked 2 packed / day. After that, the patient decided to give up smoking until this time, because of his

condition that often suffered from dyspnoe and cough. 4. Family Illness History : Mother had asthma (passed away) Sister also had asthma (passed away) 5. Family Tree :

Mother had asthma (death: 55 years old) Sister also had asthma (death: 71 years old) Patient

6. System a. Cerebrospinal b. Cardiovascular c. Respiratory d. e. f. g. h. i. j.

: : Within normal limits : Within normal limits : Barrel Chest Shape, Pulmonary ronchi +/+ wheezing +/+, pulmonary vesicular is weaken Gastrointestinal : Acute abdomen signs (-), within normal limits Urogenital : Within normal limits Musculoskeletal : Within normal limits Integument : Within normal limits Lymph nodes : Enlargement of lymph nodes (-) Eye : Cyanosis -/- Icteric sclera -/ENT : Inflammation / Infection signs (-)

C. Bio-Psycho-Social Background:

The patient lives with children and grandchildren, the wife was death, had 4 children and 4 grandchildren. D. Socio-economic Background: Economical condition is middle and lower class. E. Environmental Background: Live in dense neighborhood. F. Other Notes: G. Physical Examination On July 9, 2010 1. General Appearance : compos mentis 2. Vital Signs : BP 110/80 mmHg RR 28/min

HR 84/min 3. Nutritional status Weight/Age Height/Age Head Neck (-) Thorax Cardiac Pulmonary Abdomen Extremity

Temperature 36,7 0C

: : 159 cm : 42 kg : Cyanosis -/- Icteric sclera -/: JVP normal, enlargement of lymph nodes : Barrel chest shape : Cardiac murmur -/: Pulmonary ronchi +/+ wheezing +/+, pulmonary vesicular is weaken : within normal limits : Oedema (-)

H. Adjunct Examinations 1. Blood test Hb : WBC : L/M/N/B/E : 36/1/59/0/2 RBC : Platelet : Na : K : Cl : AST/SGOT : ALT/SGPT : 2. Urinalysis :3. Stool examination : 4. X-ray : COPD pulmonary impression, cor is not large 5. Other examination : -

I. Diagnosis
Working Diagnosis : Chronic Obstructive Pulmonary Disease (COPD) Differential Diagnosis : Chronic Bronchitis Chronic Asthma Emphysema

II. Therapy 1. Medication

: at Primary Health Care a. Pharmacology : Aminofilin 1 tab (if necessary) Methylprednisolon 0-0-1 GG 3x1 tab b. Non-pharmacology : suggestion for physiotherapy 2. Diet : High calories and proteins III. Education Avoid smocking and airpolution, prevent respiratory tract infection.

IV. Monitoring
Pulmonary function test Blood gas examination

V. Prognosis
Dubia ad bonam

VI. DISCUSSION A. Self Raising Questions & Answers 1. Definitions of Chronic Obstructive Pulmonary Disease (COPD)? COPD is a general term which covers many previously used clinical labels which are now recognized as being different aspects of the same problem Diagnostic labels encompassed by COPD include: _ chronic bronchitis _ emphysema _ chronic obstructive airways disease _ chronic airflow limitation _ some cases of chronic asthma COPD is a chronic, slowly progressive disorder characterized by airways obstruction (FEV1 <80% predicted and FEV1/FVC ratio <70%) which does not change markedly over several months The impairment of lung function is largely fixed but is partially reversible by bronchodilator (or other) therapy. Most cases are caused by tobacco smoking. COPD causes significantly more mortality and morbidity than do other causes of airflow limitation in adults. 2. Diagnosis of COPD? The diagnosis is usually suggested by symptoms but can only established by objective measurement, preferably using spirometry (see chart overleaf). Unlike asthma, airflow limitation in COPD as measured by the FEV1 can never be returned to normal values. However, treatment can improve both symptoms and measured airflow limitation. The symptoms & signs vary with the severity of the disease 3. Factors for consideration by the GP? In managing COPD, the GP needs to consider _ smoking cessation _ screening in Well-person clinics for smokers, aged 40+ _ access to spirometry _ hospital referral/follow-up 4. Indications for specialist referral A specialist opinion may be helpful at any stage of disease. The principal reasons are summarized in the table below:

5. Scheme of Diagnosis and Management of COPD?

B. Group Raising Questions 1. Q :

A : Ref :

2. Q

: A : Ref : : A : Ref : : A : Ref : : A : Ref :

3. Q

4. Q

5. Q

C. Feedbacks and answers from clinical consultant

Consultant 1 1. Ref: Consultant 2 1. Ref:

VII. REFLECTION and REVISION

LESSON LEARNT:

Primary Prevention: 1. Health Promotion - Avoid the modifiable risk factors below a. Smoking: The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking. Exposure to cigarette smoke is measured in pack-years, the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand b. Occupational exposures

Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers. Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition. The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking. c. Air pollution Studies in many countries have found that people who live in large cities have a higher rate of COPD compared to people who live in rural areas. Urban air pollution may be a contributing factor for COPD as it is thought to slow the normal growth of the lungs although the long-term research needed to confirm the link has not been done. In many developing countries indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women. - Non Modifiable risk factor : Genetics Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers. The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke. - Other risk factors A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease. It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats may be related to the development of COPD. - Autoimmune disease There is mounting evidence that there may be an autoimmune component to COPD. Many individuals with COPD who have stopped smoking have active inflammation in the lungs. The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation. This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.

2. Specific Protection - Smoking cessation - Stop Occupational exposures : avoid the Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition. The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of smoking. - Stop Air pollution : In many developing countries indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.
Secondary Prevention: 1. Early Diagnosis & Prompt Treatment

Make Diagnosis: spirometry In general, spirometry is preferred to peak expiratory flow recordings. If the latter are used, serial recordings over one week are needed to confirm the absence of variability. Many COPD patients show some degree of response to bronchodilators. A chest x-ray excludes other pathologies but cannot positively diagnose COPD.

2. Disability Limitation

Pulmonary rehabilitation including out-patient based programmes have been shown to improve exercise performance and reduce breathlessness. Depression should be identified and treated Non pharmacological : Exercise should be encouraged, Obesity or poor nutrition both require treatment, Influenza vaccination is recommended Assess social circumstances Long term O2 therapy referral to respiratory specialist for measurement of arterial blood gases. Prescribe only if PaO2 <7.3kPa

Tertiary Prevention: Rehabilitation