Management of COPD

The goal of COPD management are:

1. Touch ups the ability of people with symptoms mengatasiu not only in the acute phase, but also the chronic phase.
2. Improving the ability of the patient in carrying out daily activities.
3. Reducing the rate of progression of disease if the disease can be detected early.

Management of COPD in the elderly are as follows:

1. Etiological factors negate / precipitation, for example immediately stop smoking, avoid air pollution.
2. Cleaning the bronchial secretions to help in various ways.
3. Eradicate the infection with antimicrobial. In the absence of antimicrobial infections need not be given. Provision of appropriate antimicrobial should be in accordance with the germs that cause infections according to the results of sensitivity testing or empirical treatment.
4. Overcome bronchospasm with bronchodilator drugs. The use of corticosteroids to resolve the inflammatory process (bronchospasm) is still controversial.
5. Symptomatic treatment.
6. Treatment of the complications that arise.
7. Oxygen treatment, for those who need. Oxygen should be administered with a slow flow of 1-2 liters / minute.
8. Rehabilitation actions which include:

• Physiotherapy, mainly aims to help the expenditure of bronchial secretions.

• Breathing exercises, to train the patient in order to make the most effective breathing.

• Exercise with weights oalh particular sport, with the aim to restore physical fitness.

• Vocational guidance, the work done against the patient can re-do their previous occupation.

• Psychosocial management, primarily intended for patient self-adjustment to her illness.

 COPD (Chronic Obstructive Pulmonary Disease)

Tags : Management of COPD, COPD treatment, The goal of COPD management,

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


Tags : What Is COPD, COPD Symptoms, COPD treatment, COPD Stages, COPD Disease, Asthma COPD, COPD Pathophysiology, COPD Etiology, COPD Sign Symptoms, COPD Guidelines, COPD life expectancy

Bronchial Asthma

Bronchial asthma is a disease of the lung inflammation in the airways resulting in airway hiperrespon to various stimuli that can cause constriction of the airways that can arise thorough so shortness of breath that is reversible either spontaneously or with therapy.

Etiology

• Genetic factors
• Environmental factors
• Materials allergens
• Respiratory tract infections (especially viruses)
• Air pollution
• Food Factor

Trigger factors

• Allergens
• Physical
• Chemicals
• Infection
• Mechanical factors
• Psychological factors

Pathogenesis
The entry of allergens into the airway will cause a reaction between the allergen with immunoglobulin E. The release of materials from mastosit mediators, which cause the inflammation in the bronchial mucosa and submucosa causing bronchial smooth muscle contraction.

Pathology
Infiltration of inflammatory cells such as eosinophils, neutrophils, and other airway epithelial damage, resulting in expenditures as well as mediators and thickening of the mucosal and submucosal edema. There is hyperplasia of the glands Goblet cells. Happen "mucous plug" on-line the airways.

Clinical Symptoms
Complaints and symptoms depend on the severity at the time of the attack. In bronchial asthma attacks are mild and without complications, complaints and no typical symptoms.

Complaints:

• Breath sounds
• Crowded
• Cough

Physical examination
Abnormalities of the upper airway, bronchi, thoracic, and skins, can be rhinitis, sinusitis, bronchitis, asthma and alveoler broncho-lung hyperinflation.
General state:

• Composmentis
• Anxiety / anxiety / panic / sweating
• Blood pressure increases
• Pulse increased
• Pulsus paradoxus: decrease in systolic blood pressure over 10 mm Hg at the time of inspiration
• Respiratory frequency increased
• Cyanosis
• Auxiliary respiratory muscles hypertrophy

Lung:

• Obtained prolonged expiratory
• Wheezing

Laboratory:

• Increased blood Eosinophils> 250/mm3
• Analysis of blood gases in status asthmaticus

Radiology: there are no typical signs.
Pulmonary Physiology: decreased FEV1
Skin test: to indicate the presence of allergic
Bronchial provocation test: with inhaled histamine, acetylcholine, allergens.

Diagnosis

1. Anamnesa: complaints of shortness of breath by breath sounds ngiik frequent recurrence. The existence of hereditary factors and the presence of precipitating factors.
2. Physical examination: a thorough wheezing or prolonged expiratory phase.
3. Laboratory:

• Sputum: Charcot-Leyden crystals, Spiral Curschmann
• Blood: increased number of eosinophils.
• Physiology lung: airway obstruction (ratio of FEV1 / FVC <75% or PEF <150 liters / minute)
• bronchial provocation tests, skin sensitivity test.

Differential Diagnosis

• Upper airway obstruction (stridor)
• Laryngeal dysfunction
• Chronic obstructive pulmonary disease
• Congestive heart failure (asthma cardial)
• Pulmonary embolism
• Pulmonary infiltrates of eosinophils
• Cough caused by medications (beta blockers, ACE inhibitors).

Complications

• Respiratory infection
• Atelectasis
• Pneumothorax, Pneumomediastinum, Emphysema cutis
• Respiratory failure
• Arrhythmias (especially if previously existing cardiac abnormalities).

Management / Procedure of Bronchial asthma

Special Treatment of Bronchial Asthma


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Emphysema

Emphysema Lung Is the permanent widening of the structure of pulmonary gas exchange that is distal to the terminal bronchioles, accompanied by destruction of alveolar walls.

Etiology

1. Main factors: smokers either active smoking or passive smoking depending on the length, number, how to smoke.
2. Air pollution, in the form: Particles, These chemicals, Toxic Gas
3. Infections: viral and bacterial
4. Genetics:

a. Talent arise emphysema
b. The balance of destructive enzymes (protease) & protective enzymes (alpha-1-antitrypsin).

Google Image

Pathogenesis
Inhalation of cigarette smoke or pollutants stimulate cells in the lung macrophages and neutrophils produce elastase and collagenase is an enzyme that damages the fibers of elastin and collagen, and which is the framework of the alveoli and acini in order not to collapse. Smoking also inhibit the action of alpha-1-antitrypsin, an enzyme that protects elastin fibers against proteases.
In the lung there is a balance between destroying enzyme (protease) and protective enzymes (alpha-1-antitrypsin). Due to destruction of fibers of the lung elastin & collagen loss of elastic recoil.

Complaints and Clinical Symtomps
Progressive shortness of breath, tired easily when moving.
Pure emphysema without coughing, shortness, of breath sounds, sputum.
Breathing by means of "purse lips" aims to breathe more easily because of the onset of back pressure in the bronchioles so easy expiration and prevent "water trapping".

On physical examination found:
Chest barrel shaped chest, the space between the ribs widen.
Lung hyperinflation, the percussion sounds hipersonor, reduced chest expansion, difficulties inspiration, decreased breath sounds, rhonchi could be heard when there is phlegm.

Diagnosis
Based on anamnesa, complaints and symptoms, supplemented by investigation as follows:

• PA chest X-ray photo:

Lung looks hyperaereted.
Reduced vascular picture and not look at the third peripheral lung field, it appears the bulla, where the diaphragm is low, little heart shape in the form of water droplets.

• Tests pulmonary physiology:

Showed abnormalities obstruction.
FEV1 <80% pred. and restrictive decreased FVC <70%, RV> pred. in accordance with lung hyperinflasi

• Examination of enzymatic:

Levels of alpha-1-antitrypsin is low.

• Analysis of blood gases:

There hipercapnea hypoxemia and the alveoli as a result of capillary damage and interference ratio of ventilation / perfusion.

Differential Diagnosis

• Bronchial Asthma
• Chronic Bronchitis
• Pneumothorax

Management of Emphysema

• Prevention: stop smoking, reduce exposure to air pollution.
• There is no effective treatment and satisfactory.
• Treatment with a new bronchodilator reversibility is given when there is obstruction.
• Antibiotics are given if there are signs of respiratory tract infection.
• Oxygen increases when crowded.
• Rehabilitation of relaxation with breathing exercises, postural drainage, exercise improves breathing capacity.
• Treatment of the complications.

Complications

• Pneumothorax: outbreak caused superficial bulla
• Respiratory failure: due to bad ratio of ventilation / perfusion
• Cor pulmonale: arise due to pulmonary hypertension due to hypoxemia and pulmonary vasospasm
• Weight loss until emasiasi.

Prognosis
In emphysema caused by deficiency of alpha-1-antitrypsin bad prognosis.
Prognosis is determined by:

• The rate of progression of the emphysema
• The degree of bronchial obstruction and reversibilitasnya
• The presence of complications
• The accuracy of the management of emphysema.

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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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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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