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TITTLE CASE : COPDGroup Puskesmas (Puskesmas Mergangsan)

Participant’s :

dr. Yulaika Kusuma Wardanidr.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. Patient’s Identity

Name : Mr. SS

Sex : Male

Age : 81 years old

Height : 159 cm

Weight : 42 kg

Marital status : widower

Occupation : toys vendor (in the past)

Address : Dalem, Rt 42 Rw 10 Purbayan KotagedeExamination date : 9 July 2010

B. Anamnesis

1. Chief complaint : Dyspnoe

2. Current History : 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 hecan’t relieved in breathing.

3. Past History :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 upsmoking until this time, because of his

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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 : Within normal limits

b. Cardiovascular : Within normal limits

c. Respiratory : Barrel Chest Shape, Pulmonary ronchi +/+

wheezing +/+, pulmonary vesicular is weaken

d. Gastrointestinal : Acute abdomen signs (-), within normal

limits

e. Urogenital : Within normal limits

f. Musculoskeletal : Within normal limits

g. Integument : Within normal limits

h. Lymph nodes : Enlargement of lymph nodes (-)

i. Eye : Cyanosis -/- Icteric sclera -/-

 j. ENT : Inflammation / Infection signs (-)

C. Bio-Psycho-Social Background: The patient lives with children andgrandchildren, 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

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HR 84/min Temperature 36,7 0C

3. Nutritional status :

Weight/Age : 159 cm

Height/Age : 42 kg

Head : Cyanosis -/- Icteric sclera -/-

Neck : JVP normal, enlargement of lymph nodes

(-)

 Thorax : Barrel chest shape

Cardiac : Cardiac murmur -/-

Pulmonary : Pulmonary ronchi +/+ wheezing +/+, pulmonary

vesicular is weaken

Abdomen : within normal limits

Extremity : Oedema (-)

H. Adjunct Examinations

1. Blood testHb : -

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.

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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:

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5. Scheme of Diagnosis and Management of COPD?

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B. Group Raising Questions

1. Q :

A :

Ref :

2. Q :

A :

Ref :

3. Q :

A :

Ref :

4. Q :

A :Ref :

5. Q :

A :

Ref :

C. Feedbacks and answers from clinical consultant

Consultant 1

1.

Ref:

Consultant 2

1.

Ref:

VII. REFLECTION and REVISIONLESSON 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

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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, lessintense 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 acause 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.

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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 fromwelding 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

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- 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

Tertiary Prevention: Rehabilitation

- Assess social circumstances

- Long term O2 therapy referral to respiratory specialist for measurement of 

arterial blood gases. Prescribe only if PaO2 <7.3kPa