CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

Hey people today we will discuss about COPD . after the  end of this article you will learn about COPD s definition investigation diagnosis treatment cause and many more related to COPD.

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RESPIRATORY DISEASES

Topic :- 

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

DEFINITION

Chronic obstructive pulmonary disease (COPD) refers to a group of lung diseases that block airflow and make breathing difficult.

Emphysema and chronic Bronchitis are the two most common conditions that make up COPD. Chronic Bronchitis is an inflammation of the lining of bronchial tubes, which carry air to and from lungs. Emphysema occurs when the air sacs (alveoli) at the end of the smallest air passages (bronchioles) in the lungs are gradually destroyed.

CAUSES OF AIRWAY OBSTRUCTION

• Emphysema. This lung disease causes destruction of the fragile walls and elastic fibers of the alveoli. Small airways collapse when we exhale, impairing airflow out of lungs.

• Chronic Bronchitis. In this condition, bronchial tubes become inflamed and narrowed and lungs produce more mucus, which can further block the narrowed tubes. develop a Chronic cough trying to clear airways.

Cigarette smoke and other irritants

In the vast majority of cases, the lung damage that leads to COPD is caused by long-term cigarette smoking. But there are likely other factors at play in the development of COPD, such as a genetic susceptibility to the disease, because only about 20 percent of smokers develop COPD.

Other irritants can cause COPD, including cigar smoke, secondhand smoke, pipe smoke, air pollution and workplace exposure to dust, smoke or fumes.

Alpha-1-antitrypsin deficiency

In about 1 percent of people with COPD, the disease results from a genetic disorder that causes low levels of a protein called alpha-1-antitrypsin. Alpha-1-antitrypsin (AAt) is made in the liver and secreted into the bloodstream to help protect the lungs. Alpha-1-antitrypsin deficiency can affect the liver as well as the lungs. Damage to the liver can occur in infants and children, not just adults with long smoking histories. For adults with COPD related to AAt deficiency, treatment options are the same as those for people with more common types of COPD. Some people can be treated by replacing the missing AAt protein, which may prevent further damage to the lungs. wedamage to lungs from COPD can’t be reversed, but treatment can help control symptoms and minimize further damage.

CLASSIFICATION

COPD can be classified into three stage;

1. Mild

• Spirometry – FEV1 (60-79%)

2. Moderate

• Spirometry – FEV1 (40-59%) predicted

3. Severe

• Spirometry – FEV1 (<40%) predicted

PREDISPOSING FACTORS OF COPD

• Smoking

• Respiratory tract infection

• Genetic predisposition

• Occupational exposure (fumes)

• Sudden change in temperature

• Environmental pollution (dust, smoke etc.)

• Exposure to dampness, fog .etc.

PREDISPOSING FACTORS OF ACUTE EXACERBATION OF COPD

1. Respiratory tract infection

2. Pneumothorax

3. Left ventricular failure

4. Use of sedative drugs

5. Pulmonary embolism

RISK FACTORS

Risk factors for COPD include:

• Exposure to tobacco smoke; The most significant risk factor for COPD is long-term cigarette smoking. The more years smoke and the more packs smoke, the greater risk. Pipe smokers, cigar smokers, marijuana smokers and people exposed to large amounts of secondhand smoke also are at risk.

• People with Asthma who smoke; the combination of Asthma, a chronic airway disease, and smoking increases the risk of COPD even more.

• Occupational exposure to dusts and chemicals; Long-term exposure to chemical fumes, vapors and dusts in the workplace can irritate and inflame lungs.

• Age;COPD develops slowly over years, so most people are at least 35 to 40 years old when symptoms begin.

• Genetics; An uncommon genetic disorder known as alpha-1-antitrypsin deficiency is the source of some cases of COPD. Other genetic factors likely make certain smokers more susceptible to the disease.

CLINICAL FEATURES OF COPD

 Symptoms

• Cough ( for at least 3 months a year for 2 consecutive years

• Restless

• Breathlessness

• Sputum( scantly mucoid or perfuse mucopurulent or purulent)

• Similar attacks in past

• Chest tightness

• Lack of energy

• Unintended weight loss

• Frequent respiratory infection

 Signs

1) Vitals

• Respiratory rate increase

• Pulse rate increase and bounding

• Temperature raised or normal

• Blood pressure normal or high or low

2) General examinations

• Cyanosis

• Flapping tremor ( due to CO2 narcosis)

• Drowsy and restless (due to hypoxia)

• Reduced length of trachea palpable above the sternal notch.

• Use of accessory muscles of respiration.

• Built is thin and weak

• Tracheal tug ( trachea descend during inspiration)

• Features of right heart failure:

- Raised JVP

- Hepatomegaly

- Pedal oedema

3) Chest examination

 Inspection

• Prominent accessory muscles of respiration

• Hyper inflated chest, increased antero-posterior diameter of chest

• Excavation of the suprasternal and supraclavicular fossae during inspiration.

• Indrawing of the costal margins and intercostal spaces. 

 Palpation

• Tracheal tug

• Diminished chest expansion

• Decreased length of palpable trachea above sternal notch.

 Percussion

• Hyper-resonance of lung field

 Auscultation:

• Vesicular breathing sounds with prolonged inspiration

• Rhonchi (inspiratory and expiratory)

• Crepitations when there is associated chest infection

• Cardiac murmur ( tricuspid regurgitation: pansystolic murmur in tricuspid area)

INVESTIGATIONS

 Chest X-Ray PA view

Findings: -Tubular heart

- Hyper inflated lung field of chronic obstructive pulmonary disease.

- Low flat diaphragm

- Emphysematous bulla

- Pneumothorax ( complication)

- Associated chest infection

 Blood: - Hb% increased

- ESR increased

- TC,DC,( leucocytosis)

 Sputum:

- Gram stain

- Culture and sensitivity (C/S)

- AFB staining

 Spirometry:

- Reduced forced expired volume in 1 second

- Increased Residual Volume (RV)

- Increased Total Lung Capacity ( TLC)

- Reduced forced expired volume and vital capacity ratio. ( FEV1< 80% FEV1/VC <70%)

- Arterial blood gas analysis

 Hypoxia and hypercarbia (High CO2)

 ECG:

- P- pulmonale ( height of P – wave more than 2.5 mm in lead ii)

- Right ventricular hypertrophy

 Echocardiography:

- Right atrium and right ventricle enlargement

- Tricuspid regurgitation

TREATMENT

   (ABCD-O2)

a) Antibiotic therapy

b) Bronchodilators

c) Corticosteroids

d) Postural Drainage

e) O2 therapy

MANAGEMENT

A. Reduction of bronchial irritation: e.g, cessation of smoking

B. O2 therapy: O2 therapy improves survival and quality of life in patient with chronic hypoxiaemia or cor-pulmonale.

C. Bronchodilators:

 Ipratropium bromide

 Short acting B2 agonists

 Theophyllines and its derivatives.

DRUGS:

• Amoxicillin 250-500mg 8- hourly or

• Clarithromycin 250-500mg 12- hourly or

• Cortimoxazole 960mg 12- hourly

Durationof antibioticstherapy 7-10 days.

COMPLICATIONS

• Pulmonary hypertension

• Chronic respiratory failure

• Acute exacerbation of chronic obstructive pulmonary disease

• Cor- pulmonale

• Brochopulmonary mycosis

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