COPD (Chronic Obstructive Pulmonary Disease)

COPD(Chronic Obstructive Pulmonary Disease) is a broad classification of disorders that includes chronic bronchitis, bronchiectasis, emphysema and asthma, which is an irreversible condition associated with dyspnea on exertion and decreased air flow in and out of the lungs.
Chronic obstructive pulmonary disease is a disease that causes airway obstruction, including therein is asthma, chronic bronchitis and emphysema Pulmonum.
Chronic obstructive pulmonary disease is a lung disorder characterized by impaired lung function in the form of prolonged expiratory period caused by the narrowing of the airways and not much changed in the period of observation for some time.
Disease chronic obstructive lung is a term used for a group of lung diseases that last long and is characterized by increased resistance to air flow as the main pathophysiological picture.

Classification
Diseases included in chronic obstructive pulmonary disease group are as follows:
1. Chronic Bronchitis
Bronchitis is a clinical definition to cough almost every day accompanied by sputum expenditure, at the lack of 3 months in a year and occurred at least 2 consecutive years.
2. Pulmonary emphysema
Pulmonary emphysema is an anatomic definition, namely a change of anatomic lung characterized by abnormal widening of the distal bronchial airways terminalis, which is accompanied by alveolar wall destruction.
3. Asthma
Asthma is a disease characterized by hypersensitivity tracheobronchial branches of various types of stimuli. This condition manifests as narrowing the channels of periodic breathing due to bronchospasm and reversible.
4. Bronchiectasis
Bronchiectasis is a chronic dilatation of bronchi and bronchioles yan may be caused by various conditions, including pulmonary infections and bronchial obstruction, foreign body aspiration, vomit, or the objects of the upper respiratory tract, and the pressure of the tumor, which dilates blood vessels and lymph node enlargement.

Etiology
The etiology of this disease is unknown. The disease is associated with the risk factors contained in people include:
1. Cigarette smoking is a long
2. Air Pollution
3. Peru recurrent infections
4. Age
5. Gender
6. Race
7. Alpha-1 antitrypsin deficiency
8. Deficiency of anti-oxidants
The effect of each risk factor for COPD is the occurrence of mutually reinforcing factors and smoking are considered the most dominant.

Pathophysiology
Lung function decline with the advent of old age are caused by elasticity of lung tissue and chest wall dwindle. In a more advanced age, the strength of respiratory muscle contraction can be reduced making it difficult to breathe.
Lung function to determine a person's oxygen consumption, ie the amount of oxygen bound by blood in the lungs to the body uses. Oxygen consumption is closely related to blood flow to the lungs. Reduced lung function is also caused by reduced function of the respiratory system such as pulmonary ventilation function.
Risk factors mentioned above will bring the process of bronchial inflammation and bronchial wall damage apda terminalis. Damage will occur as a result of the small bronchial obstruction (terminal bronchioles), which experienced early closure or obstruction of expiratory phase. The air that easily fit into the alveoli during inspiration, during expiration many trapped in the alveoli and there was a buildup of air (air trapping). This has led to complaints of shortness of breath with all its consequences. Obstruction in the early expiration will cause trouble and cause a lengthening expiratory expiratory phase. Pulmonary functions: ventilation, gas distribution, gas diffusion, and perfusion of blood will have the disorder (Brannon, et al, 1993)

Examination Support
Investigations required are as follows:
A. Radiological Examination
In chronic bronchitis radiological there are some things to note:

1. Tubular shadows or farm lines visible shadow lines are parallel, out from the hilum toward the lung apex. The shadow is the shadow of a thickened bronchus.
2. Pattern of increased lung

In pulmonary emphysema there are two forms of abnormal chest images are:

1. Picture of arterial deficiency, occurs overinflasi, pulmonary oligoemia and bullae. This situation is more often found in panlobular emphysema and pink puffer.
2. Pattern lung is increased.

B. Examination of Lung Physiology
In chronic bronchitis there is a KV VEP1 and declining, VR is growing and a normal ID card. In pulmonary emphysema there is a decrease VEP1, KV, and KAEM (arum expiratory maximum speed) or MEFR (maximal expiratory flow rate), KRF and VR increases, whereas KTP increased or normal. The situation above is more clearly at an advanced stage, being at an early stage changes only to the small airways (small Airways). In emphysema decreased diffusion capacity of the alveoli due to surface diffusion is reduced.

C. Blood Gas Analysis
In bronchitis PaCO2 increased, decreased hemoglobin saturation, arise cyanosis, pulmonary vascular vasoconstriction occurs and the addition eritropoesis. That chronic hypoxia stimulate erythropoietin formation, giving rise to polycythemia. At the age of 55-60 years polycythemia conditions causing right heart must work harder and is one of the causes of right heart trouble.

D. ECG
Abnormalities of the earliest was a clock wise rotation of the heart. If there is a cor pulmonale was found to right axis deviation and P pulmonale on delivery II, III, and aVF. Low QRS voltage ratio in V1 R / S is more than 1 and V6 ratio R / S is less than 1. There are often incomplete RBBB.

E. Cultures of sputum, to determine the cause of infection petogen.


F. Complete blood laboratory


Management of COPD


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Special examination of Chronic bronchitis

Special examination :

•  X-ray photo PA and left lateral chest

-  Typically show no abnormalities, except when it occurs cor pulmonale or emphysema.
-  It may also seem an increase in "bronchovascular markings".

• Sputum: direct smear, Gram staining.

Please note: the existence of cells in sputum, whether the material is indeed contaminated with sputum or saliva from the oropharynx. Sputum can be identified because of alveoler macrophages (histiocytes). Macrophages alveoler this form round cells, large, with eccentric nuclei and oval or kidney-shaped near the edge of the cell.
Tues skuamus flat and very large and has a spherical nucleus in the middle. If there were> 25 epithelial cells in sputum skuamus, means contaminated with saliva or secretions from the oropharynx.
In chronic bronchitis who experience eksaserbrasi yellow sputum, bronchial ciliated epithelium that despite apparent in sputum neutrophil and looks.
At the time of remission decreased number of neutrophils, but macrophages alveoler increased, resulting in mucoid sputum and grayish-white color.
When sputum is contaminated, it should be repeated sputum collection or rinsed with water (washed sputum), a new Gram staining was made. Note the presence of neutrophils and bacteria. If the bacteria seemed gather very much and the same morphology, mean as a result of stasis, so sputum should be discarded. If it seems a variety of bacteria and many in the sputum, saliva possible, should be attempted again looking for new specimens. Look for the etiology of bronchial inflammation.

• If the Gram-positive cocci in pairs or forming short chains means "Streptococcus pneumoniae" (diplococus).
• If the Gram-positive cocci and form large clusters, meaning "Staphylococci".
• Basil Gram-negative, such as haemophilus influenza, Seratia, Pseudomonas, Klebsiella, E. Colli, and others.

Guidelines for assessment of sputum on COPD:

1. Gram staining of pus cells --> <1-5  inflammation (-) and germs (-); seed germ (+) --> not the cause of the disease.
2. Gram staining (+) and seed (+) --> possible causes of infection.
3.  Gram staining (-) and seed a little (+) --> sputum contaminated with saliva.

If the sputum culture results did not confirm the results of gram staining on sputum smears are true, then breeding considered untrustworthy. If the breeding is not the same as the results of gram staining, a new specimen should be made when antibiotics are used not deliver results.

Tests pulmonary physiology:
To determine the presence of airflow obstruction in chronic bronchitis, pulmonary physiology need to check:

• FVC (Forced Vital Capacity)
• FEV1 (Forced expiratory volume one second)
• FEF 25-75% (Forced expiratory flow over the mid - 50% of the vital capacity) to detect obstruction in small airways.
• PEFR (peak expiratory flow rate), only to find out the existence of a large obstruction in the airway, can be done in the clinic.
• TLC (Total Lung Capacity), can only be examined at a hospital that has a complete facility in the form of "body plethysmograph or by helium dilution or nitrogen washout method technique".

In chronic bronchitis:

• VC is normal or decreased (<80%)
• FEV1 is normal or decreased (<80%)
• FEV1 / FVC is always decreased (<75%)
• FEF 25-75% was always decreased (<80%)
• TLC normal / increased (N = 80-120%)
• RV / TLC% is always increasing (N = 25-40%)

Pulmonary Physiology showed obstruction

• ECG is necessary to know the existence of right heart hypertrophy, such as in cronic cor pulmonale.
• Examination Arterial Blood Gases:

- PaO2 decreased to 70-80%, normal 80-100 mm Hg.
- PaCO2 normal / increased to 25-35%. Normal = PaCO2 = 35-45 mm Hg.
- pH is normal or decreased (when the state information). Normal pH = 7.35 to 7.45.

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Chronic Bronchitis

Chronic bronchitis is a disease, characterized by cough with phlegm every day, at least 3 months per year and lasts for 2 consecutive years, and the absence of other diseases with symptoms.

Etiology and pathogenesis
Etiology

• Exposure to cigarette smoke, both at the "smoker" or "passive smoker". For the smoker is usually measured by pack year (pack years).
• Exposure to contaminated air in workplaces (eg dust or gas from industrial or workplace).
• Social factors and residential solid and air pollution in the settlement area by the gases SO2 and NO2.
• Respiratory tract infection by the virus will cause eksaserbrasi chronic bronchitis. For example, by class sinsisial respiratory viruses and influenza virus group.
• Most bacteria that are found in chronic bronchitis are streptococcus pneumonia and haemophilus influenza.

Pathogenesis

a. Cigarette smoke is a disincentive to the bronchial mucosa, to changes:

• Lung Defense:

1. Purge function mukosilia slow,
2. Alveoler Macrophage numbers are increasing,
3. Impaired macrophage function,
4. The process of antigen and antigen response to change.

• Small airways:

1. Inflammation,
2. The increased muscle,
3. Fibrosis,
4. Refinement,
5. The number of goblet cells increases.

• Alveoli:

1. The number of neutrophils, macrophages increased,
2. Emphysema.

b.  Exposure to air polluted by industrial pollution or the disposal of fuel combustion in motor vehicles:

1. Sulfur dioxide (SO2) and the complex particles (<10 u), derived from: Fossil fuels, power generation, oil refining, tobacco smoke, kerosene heaters, stoves that use wood or coal fuel. These materials cause bronchoconstriction.
2. Photochemical oxidants, nitrogen oxides, ozone, produced by burning fuel in motor vehicles, power plants, and solar radiation. These materials cause stimulation of the respiratory tract, impaired pulmonary physiology and impaired pulmonary defense.
3. Carbon monoxide (CO) generated by the combustion of automotive fuel, cigarette smoke. CO causes tissue hypoxia, especially the cardiovascular and nervous systems.

Clinical Symtoms

• Chronic cough with phlegm mucus, thick, a lot, especially in the morning. Muko-purulent sputum, or purulent if there is infection. These symptoms for cough are considered regular smokers.
• Shortness of breath with breath sounds due to progressive inflammation and bronchial obstruction.
• If the disease has continued to grow, especially shortness of running time.
• Physical examination performed on the patient sitting position:
• Chest hyperinflation 
• Percussion hipersonor
• wet crackles at the time of inspiration
• Wheezing on expiration time.

Special examination of Chronic bronchitis

Management Of Chronic bronchitis

Diagnosis
Diagnosis of chronic bronchitis is based on:

1. Anamnesa according to the criteria of chronic bronchitis with symptoms of chronic cough and phlegm, especially in the early morning, thick sputum and numerous. Sometimes purulent, especially in heavy smokers. Shortness of breath during activity and occurs slowly but progressively.
2. Physical examination is not typical, usually chest hyperinflation, hipersonor, wet crackles and sometimes audible wheezing.
3. Chest X-ray photo showed lung hyperinflation with increased bronchovascular markings.
4. Examination of sputum Gram to detect bacterial infection in exacerbation.
5. Lung physiology tests to detect obstruction or restriction.
6. ECG to determine heart abnormalities.
7. Arteriel blood gas analysis to detect hypoxemia and hypercapnea.

Differential Diagnosis

• Bronchial Asthma
• Pulmonary Emphysema
• Bronchiectasis 
• Lung Carcinoma
• Cystic fibrosis
• Pulmonary Tuberculosis.

Complications

• Exacerbation acute respiratory tract infections, pneumonia.
• Pulmonary Emphysema
• respiratory failure
• Cor pulmonale.

Prognosis

• Depending on the early treatment before the disorder is advanced lung physiology and the presence or absence of complications of emphysema and cor pulmonale.
• Stop smoking, avoid air pollution and socio-economic improvement of the patient will improve prognosis.

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Management of Chronic Bronchitis

General:

• Education to patients and their families
• Stop smoking and avoid air pollution
• Prevent infection
• Clean environment
• Hydration moderation: drink enough water (8-10 glasses a day)
• Proper nutrition: protein rich diet and avoid heavy meals before bedtime, milk can cause increased bronchial secretions, should be prevented.

Provision of drugs:
1. Bronchodilators:

• Aminophylline inj. 5.6 mg / kg i.v. or oral loading dose of 3 x 100-200 mg.
• Terbutaline 3 x 2.5 mg oral or injection 0.25 mg s.c. every 4-6 hours (1 mg / ml; = 2 ml ampoule).
• 3 x 2 mg salbutamol orally.

2. Expectorant:

• Water is a good expectorant
• Glyceryl guaiacolate 4 x 100-200 mg.

3. Mucolytic :

• Bromhexine HCL: 3 x 1 tablet by mouth.
• N-acetyl cysteine: 3 x 200 mg orally.

4. Respiratory therapy:

• Aerosols: Ipratropium Bromide 3 x 2 puffs
• Oxygen: 1-2 liters / minute via nasal cannula if PaO2 <55 mm Hg.

5. Rehabilitation:

• Physiotherapy
• Relaxation exercises
• Breathing exercises
• Chest percussion and postural drainage
• Exercise physical abilities
• Psychosocial Rehabilitation
• Vocational Rehabilitation.

Tags : Bronchitis Chronic, Management Chronic bronchitis, bronchitis treatment, 

Bronchiectasis

Bronchiectasis is abnormal and permanent dilatation of bronchi and cartilaginous being, accompanied by destruction of muscle and elastic components of the walls.

Etiology and pathogenesis
A bronchial wall inflammation, causing damage and dilatation. Contributing factors are:

1. Infection: primary and secondary.
Primary or secondary infection, either repeatedly or continuously, by: bacteria, viruses, mycoplasma, and mycobacterial clearance mukosilia and will damage the airway epithelium.
In children is often caused by: measles, whooping cough, severe pneumonia or aspiration. Primary tuberculosis is often also leads to bronchiectasis.

Endobronchial tuberculosis causing necrosis, focal stenosis due to endobronchial inflammation, enlarged lymph nodes give emphasis or endobronchial obstruction, and scarring of the parenchyma causes distortion of the airway.

2. Inhalation of toxic chemicals or materials imunoaktif.
Inhalation of toxic chemicals or materials imunoaktif or autoimmune reaction: anhydrous ammonia vapor, sulfur oxides, talc, cork, bakelite, and smoke. Aspiration of gastric contents resulting in inflammation and result in bronchiectasis, for example in the hiatal hernia, gastric motility disorders, divertikuli, trakeoesofageal fistula.

3. An abnormal immune response: a genetic or acquired.
Abnormal immune response: a genetic or "acquired".
Swollen lungs because of heroin or heroin poisoning can cause bronchiectasis, due to changes in immunological defense.
Bronchiectasis occurs in patients with ulserosa colitis, rheumatoid arthritis, Sjogren's syndrome, cutaneous vasculitis, Hashimoto's thyroiditis, pernicious anemia, "primary biliary cirrhosis," "celiac disease", and sarcoid, because of an abnormal immunological manifestations, which often form hiperresponsif or autoimmune response.
4. Mechanical factors.
Atelectasis or parenchymal fibrosis can lead to bronchiectasis. Atelectasis can cause bronchial dilatation is back to normal when the lungs expand again. Parenchymal fibrosis can lead to bronchial dilation through withdrawal.
Bronchial dilatation and distortion may interfere with clearance mukosilier, leads to accumulation of secretions, resulting in infection with bronchial wall damage elements --> bronchiectasis.

5. Inherited or congenital abnormality.
Deficiency of alpha-1-antitrypsin causes emphysema panasinar and diffuse bronchiectasis.

• "Allergic bronchopulmonary aspergillosis" --> central or proximal bronchiectasis.
• BEAP syndrome (bronchiectasis, eosinophilia, asthma, and pneumonitis).
• Bronchiectasis is a picture that stands out in cystic fibrosis, in children and adults.
• Kartegener syndrome (bronchiectasis, sinusitis, site inversus).
• Young's syndrome: obstructive Azoospermia and lung abnormalities (bronchiectasis).
• "Pulmonary sequestration".
• Yellow nail syndrome.
• William Syndrome - Campbell (deficiency of bronchial cartilage generation 4 through 8).
• Swyer Yndrome - James and Mac Leod (hipertensi unilateral lung).
• Marfan's syndrome.

Clinical Symtomps and Diagnosis Bronchiectasis

Management of Bronchiectasis

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