COPD vs RLD

Review of Lung Anatomy and Physiology

Which is the correct order of largest diameter to smallest diameter? a) primary bronchi -> secondary bronchi > tertiary bronchi -> alveoli b) alveoli -> primary bronchi -> secondary bronchi -> tertiary bronchi c) tertiary bronchi -> secondary bronchi > primary bronchi -> alveoli d) all are the same size

Review of Lung Anatomy and Physiology

Which is the correct order of largest diameter to smallest diameter? a) primary bronchi -> secondary bronchi -> tertiary bronchi -> alveoli b) alveoli -> primary bronchi -> secondary bronchi -> tertiary bronchi c) tertiary bronchi -> secondary bronchi > primary bronchi -> alveoli d) all are the same size

 How

many lobes do the right and left lung have? a) right -> 2, left -> 3 b) right -> 3, left -> 2 c) right -> 2, left -> 1 d) right -> 1, left -> 2

 How

many lobes do the right and left lung have? a) right -> 2, left -> 3 b) right -> 3, left -> 2 c) right -> 2, left -> 1 d) right -> 1, left -> 2

 How

many alveoli are found in the lung? a) 100 million b) 200 million c) 250 million d) 300 million

 How

many alveoli are found in the lung? a) 100 million b) 200 million c) 250 million d) 300 million

 What

anatomic structure lies beneath the lungs? a) trachea b) bronchi c) diaphragm d) larynx

 What

anatomic structure lies beneath the lungs? a) trachea b) bronchi c) diaphragm d) larynx

 When

the trachea comes to a fork in to road, this is called the ______? a) larynx b) epiglottis c) lungs d) bronchial tubes

 When

the trachea comes to a fork in to road, this is called the ______? a) larynx b) epiglottis c) lungs d) bronchial tubes

T or F Individual diseased lobules of the lungs can be surgically removed because major blood vessels and bronchi do not cross the connective tissues of the lung. T or F The alveoli split into numerous number of generations. T or F Surfactant reduces the surface tension at the respiratory membrane. Without surfactant the alveoli would collapse on expiration. The pulmonary vein carries ______ to the heart. a) oxygenated blood b) unoxygenated blood

Which cells make surfactant? a) type I cells b) type II cells c) WBC d) RBC The tracheal bifurcation is located: a) manubriosternal notch, 2nd rib b) 4th rib c) at the costochondral junction d) 1.5 inches above the clavicle

COPD
Definition

of COPD Classification and Epidemiology of COPD Causes of COPD Signs and Symptoms of COPD Diagnosis of COPD Management of COPD

Restrictive Lung Disease

Definition

of RLD Classification and Epidemiology of RLD Causes of RLD Signs and Symptoms of RLD vs COPD Management of COPD

Chronic Obstructive Pulmonary Disease

characterized

by the presence of airflow obstruction which is generally progressive chronic bronchitis or emphysema may be accompanied by airway hyperreactivity may be partially reversible

Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years (other causes of cough being excluded). Emphysema is defined as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.

 Based

on pooled data from a number of studies, global prevalence of COPD was 7.5% (2006)

chronic bronchitis alone was 6.4% emphysema alone was 1.8%

> F; 40-69 years old M > F in terms of mortality

Chronic Bronchitis - Pathology

Mucous gland enlargement is the histologic hallmark Structural changes include: atrophy of airways, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening Neutrophilic infiltrates accumulate in the submucosa Respiratory bronchioles mononuclear inflammatory process, lumen occlusion by mucous plugging, goblet cell metaplasia, smooth muscle hyperplasia, and distortion due to fibrosis => airflow limitation by allowing airway walls to deform and narrow the airway lumen.

Emphysema - Pathology

3 morphologic patterns

centriacinar emphysema
focal destruction limited to the respiratory bronchioles and the central portions of acinus. associated with cigarette smoking; most severe in the upper lobes.

panacinar emphysema
involves the entire alveolus distal to the terminal bronchiole Most severe in the lower lung zones and generally develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency

distal acinar emphysema or paraseptal emphysema

least common form and involves distal airway structures, alveolar ducts, and sacs localized to fibrous septa or to the pleura and leads to formation of bullae may cause pneumothorax.

Causes of COPD
Smoking

Air

pollution Airway hyperresponsiveness Alpha-1-antitrypsin deficiency

Only known genetic factor for COPD <1% incidence in the US

Most patients with COPD have smoked at least 20 cigarettes per day for 20 or more years commonly occurs in the fifth decade of life Common symptoms in the history of a patient:

A productive cough or an acute chest illness; cough usually is worse in the mornings and produces a small amount of colorless sputum. Breathlessness is the most significant symptom, but it usually does not occur until the sixth decade of life. Wheezing may occur in some patients Disease progression intervals between acute exacerbations become shorter; cyanosis and right heart failure may occur. Anorexia and weight loss worse prognosis

The RR increases proportionally to disease severity.

use of accessory respiratory muscles and paradoxical indrawing of lower intercostal spaces cyanosis, elevated jugular venous pulse (JVP), and peripheral edema FET of more than 6 seconds indicates considerable expiratory flow obstruction (ie, FEV1/forced vital capacity (FVC) <50%). hyperinflation (barrel chest) wheezing, diffusely decreased breath sounds, hyperresonance on percussion prolonged expiration. coarse crackles beginning with inspiration and wheezes frequently are heard on forced and unforced expiration

Measurement of forced expiratory time (FET) maneuver

Thoracic examination reveals:

Diagnoses

Imaging Studies

Chest radiograph
Frontal and lateral chest radiographs reveal signs of hyperinflation, including a flattening of the diaphragm, increased retrosternal air space, and a long narrow heart shadow. Rapid tapering vascular shadows accompanied by hyperlucency of the lungs are signs of emphysema. prominent hilar vascular shadows with possible right ventricular enlargement and opacity in the lower retrosternal air space pulmonary hypertension

Computed tomography scan

High-resolution CT (HRCT) scan is more sensitive than the standard chest radiograph. HRCT scan is highly specific for diagnosing emphysema, and the outlined bullae are not always visible on a radiograph. This information does not alter therapy; therefore, a CT scan is not useful in the routine care of patients with COPD.

Pulmonary function tests

essential for the diagnosis and assessment of the severity of disease; helpful in following its progress. FEV1 is a reproducible test and is the most common index of airflow obstruction. Lung volume measurements may document an increase in total lung capacity, functional residual capacity, and residual volume. The vital capacity decreases. Carbon monoxide diffusing capacity is decreased in proportion to the severity of emphysema.

Arterial blood gases reveal mild-to-moderate hypoxemia without hypercapnia in the early stages. As the disease progresses, hypoxemia becomes more severe and hypercapnia supervenes.

Management
goal

of management: improve daily living and the quality of life by preventing symptoms and the recurrence of exacerbations by preserving optimal lung function. educate the patient about the disease and encourage the patient to participate actively in therapy.

 Smoking

cessation continues to be the most important therapeutic intervention.

smoking cessation plan essential part of a comprehensive management plan low success rates addictive power of nicotine, the conditioned response to smoking-associated stimuli, and psychological problems, including depression, poor education, and forceful promotional campaigns by the tobacco industry.

Oral and inhaled medications are used for patients with stable disease to reduce dyspnea and improve exercise tolerance. Most of the medications employed are directed at 4 potentially reversible causes of airflow limitation in a disease state that has largely fixed obstruction:
(1) (2) (3) (4)

bronchial smooth muscle contraction bronchial mucosal congestion and edema airway inflammation increased airway secretion.

Medications

Inhaled steroids

Decrease frequency and severity of exacerbations; slows rate of decline of COPD

Methylxanthines, B2 agonists Ipratropium bromide

Bronchodilators

Anti-cholinergic agents

Phosphodiesterase IV inhibitors

Reduction of inflammatory response; nausea is the principal adverse reaction Cilomilast

Antibiotics

Prevent infection from Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis Patients who benefited most were those whose exacerbations were characterized by at least 2 of the following: increases in dyspnea, sputum production, and sputum purulence

Mucolytics N-acetylcysteine Oxygen therapy

Specialists recommend long-term oxygen therapy for patients with a PaO2 of less than 55 mm Hg, a PaO2 of less than 59 mm Hg with evidence of polycythemia, or cor pulmonale

Surgical Care

Bullectomy Lung volume reduction surgery

candidates for LVRS have symptoms secondary to severe emphysema, marked hyperinflation), and CT scan evidence of heterogeneous emphysema resect 20-30% of each lung from the upper zones. mortality rate of 0-18% with complications, including pneumonia and prolonged air leaks patients selected to receive a transplant should have a life expectancy of 2 years or less due to COPD.

Lung transplantation

Other forms of Management

Diet

Inadequate nutritional status associated with low body weight in patients with COPD is associated with impaired pulmonary status, reduced diaphragmatic mass, lower exercise capacity, and higher mortality rates

 The

American Thoracic Society (ATS) has recommended the clinical staging of COPD severity according to lung function.

Stage I is FEV1 of equal or more than 50% of the predicted value Stage II is FEV1 35-49% of the predicted value Stage III is FEV1 less than 35% of the predicted value.

 The

predictors of mortality

Aging Continued smoking Accelerated decline in FEV1 Moderate-to-severe airflow obstruction, Poor bronchodilator response Severe hypoxemia Hypercapnia, Development of cor pulmonale Overall poor functional capacity.

Pulmonary Rehabilitation

A multidisciplinary team approach

physician, dietitian, nurse, respiratory therapist, exercise physiologist, physical therapist, occupational therapist, recreational therapist, cardiorespiratory technician, pharmacist, psychosocial professionals

Emphasizes patient and family education, smoking cessation, medical management (eg, oxygen, immunization), respiratory and chest physiotherapy, physical therapy with bronchopulmonary hygiene, exercise, vocational rehabilitation, and psychosocial support

Components of pulmonary rehabilitation

outpatient setting tailored to the needs of the individual patient. provide all patients who complete the program with guidelines for continuing at home

Education is key to comprehensive pulmonary rehabilitation. The educational component prepares the patient and families to be actively involved in providing care. This reliance on patients to assume charge of their care is known as collaborative selfmanagement. Exercise training is a mandatory component of pulmonary rehabilitation.

aerobic lower extremity endurance exercises regularly to enhance performance of daily activities and reduce dyspnea. Upper extremity exercise training improves dyspnea and allows increased activities of daily living requiring the use of upper extremities.

Breathing retraining techniques (eg, diaphragmatic, pursed lip breathing) may improve the ventilatory pattern and prevent dynamic airway compression.

Restrictive Lung Disease

characterized by reduced lung volume due to:

alteration in lung parenchyma disease of the pleura, chest wall, or neuromuscular apparatus
reduced total lung capacity (TLC), vital capacity, or resting lung volume. Accompanying characteristics are preserved airflow and normal airway resistance, which are measured as the functional residual capacity (FRC).

In physiological terms:

Classification

Intrinsic lung diseases or diseases of the lung parenchyma

inflammation or scarring of the lung tissue (interstitial lung disease) or result in filling of the air spaces with exudate and debris (pneumonitis). characterized according to etiological factors Includes idiopathic fibrotic diseases, connective tissue diseases, drug-induced lung disease, and primary diseases of the lungs

Extrinsic disorders or extraparenchymal diseases

Chest wall, pleura, and respiratory muscles Result in lung restriction, impaired ventilatory function, and respiratory failure (eg, nonmuscular diseases of the chest wall, neuromuscular disorders)

Epidemiology

Kyphoscoliosis is a common extrinsic disorder. It is associated with an incidence of mild deformities amounting to 1 case per 1000 persons, with severe deformity occurring in 1 case per 10,000 persons For intrinsic lung diseases, studies cite an overall prevalence of 3-6 cases per 100,000 persons, with a prevalence of idiopathic pulmonary fibrosis (IPF) of 27-29 cases per 100,000 persons.

Causes of RLD

Intrinsic lung diseases

Collagen vascular diseases, including scleroderma, polymyositis, dermatomyositis, systemic lupus erythematosus, rheumatoid arthritis, and ankylosing spondylitis, are a cause of restrictive lung disease. drugs and other treatments (eg, nitrofurantoin, amiodarone, gold, dilantin, bleomycin, bischloroethylnitrosourea [BCNU or carmustine], cyclophosphamide, methotrexate, radiation). primary or unclassified diseases may include sarcoidosis, pulmonary histiocytosis X, LAM, pulmonary vasculitis, alveolar proteinosis, eosinophilic pneumonia, and BOOP. Inorganic dust exposure (eg, silicosis, asbestosis, talc, pneumoconiosis, berylliosis, hard metal fibrosis, coal worker's pneumoconiosis) may cause restrictive lung disease. Organic dust exposure (eg, farmer's lung, bird fancier's lung, bagassosis, and mushroom worker lung, which all cause hypersensitivity pneumonitis) is another cause. Idiopathic fibrotic disorders: These may include acute interstitial pneumonia, IPF (usually interstitial pneumonitis), lymphocytic interstitial pneumonitis, desquamative interstitial pneumonitis, and nonspecific interstitial pneumonitis.

Causes of RLD

Extrinsic disorders

Nonmuscular diseases of the chest wall, in which kyphosis can be idiopathic or secondary, may cause restrictive lung disease. The most common cause of secondary kyphoscoliosis is neuromuscular disease (eg, polio, muscular dystrophy). Fibrothorax, massive pleural effusion, morbid obesity, ankylosing spondylitis, and thoracoplasty are other causes. Neuromuscular diseases manifest as respiratory muscle weakness and are due to myopathy or myositis, quadriplegia, or phrenic neuropathy from infectious or metabolic causes.

Pathology
In

cases of intrinsic lung disease reduction in all lung volumes; expiratory airflow is reduced in proportion to lung volume.

Arterial hypoxemia due to V/Q mismatch; impaired diffusion of oxygen which contributes a little towards hypoxemia at rest but is primarily the mechanism of exercise-induced desaturation.

Hyperventilation

at rest and exercise

In cases of extrinsic disorders of the pleura and thoracic cage reduced lung compliance, and, hence, lung volumes are reduced; gas distribution is nonuniform, resulting in ventilation-perfusion mismatch and hypoxemia.

In kyphoscoliosis, the Cobb angle is an indication of the severity of disease. An angle greater than 100 is usually associated with respiratory failure. neuromuscular disorders respiratory pump can be impaired at the level of the central nervous system, spinal cord, peripheral nervous system, neuromuscular junction, or respiratory muscle.

careful history of occupation, travel, habits, hobbies, exposures, and HIV risk factors is critical to help identify any etiologic agent. Duration of illness, smoking history, medication history, occupational and environmental exposure

Symptoms of intrinsic diseases

Progressive exertional dyspnea is the predominant symptom. Grading the level of dyspnea is useful as a method to gauge the severity of the disease and to follow its course. A dry cough is common and may be a disturbing sign. A productive cough is an unusual sign in most patients with diffuse parenchymal lung disorders. Hemoptysis or grossly bloody sputum occurs in patients with diffuse alveolar hemorrhage syndromes and vasculitis. Wheezing is an uncommon manifestation but can occur in patients with lymphangitic carcinomatosis, chronic eosinophilic pneumonia, and respiratory bronchiolitis. Chest pain is uncommon in most instances of the disease, but pleuritic chest pain can occur in patients with rheumatoid arthritis, systemic lupus erythematosus, and some drug-induced disorders

Symptoms of extrinsic disorders

Nonmuscular diseases of the chest wall affect patients with kyphoscoliosis. Patients younger than 35 years tend to be asymptomatic, whereas middle-aged patients develop dyspnea, decreased exercise tolerance, and respiratory infections. The cause of respiratory failure is often multifactorial and is secondary to spinal deformity, muscle weakness, disordered ventilatory control, sleep disordered breathing, and airway disease. Neuromuscular disorders occur as the respiratory muscle weakness progresses. Patients develop dyspnea upon exertion, followed by dyspnea at rest, and their condition ultimately advances to respiratory failure. Acute and chronic respiratory failure, pulmonary hypertension, and cor pulmonale eventually ensue.

chest wall disorders show obvious massive obesity and an abnormal configuration of the thoracic cage (eg, kyphoscoliosis, ankylosing spondylitis). Abnormal breath sounds:

Velcro crackles (interstitial lung disorders) Inspiratory squeaks or scattered, late, inspiratory high-pitched rhonchi (bronchiolitis)

Cyanosis at rest is a late manifestation of advanced disease. Digital clubbing is common in those with IPF and is rare in others (eg, those with sarcoidosis or hypersensitivity pneumonitis). Extrapulmonary findings, including erythema nodosum, suggest sarcoidosis. A maculopapular rash can occur in those with connective tissue diseases, or it may be drug-induced. Raynaud phenomenon may be present in patients with connective tissue diseases, and telangiectasia is present in those with scleroderma. Peripheral lymphadenopathy, salivary gland enlargement, and hepatosplenomegaly are signs of systemic sarcoidosis. Cor pulmonale occurs in the late stages of pulmonary fibrosis or advanced kyphoscoliosis. Pulmonary hypertension and cor pulmonale a loud P2, right-sided precordial lift, and right-sided gallop.

Diagnosis
Depends

on the underlying cause Blood chemistry and serum markers Imaging Modalities (CXR, CT scan) Pulmonary function tests

All disorders are associated with a restrictive defect with a reduction in TLC, FRC, and residual volume (RV).

Bronchoalveolar
Biopsy

lavage

Management
Treatment

depends on the specific diagnosis, which is based on findings from the clinical evaluation, imaging studies, and lung biopsy. Corticosteroids, immunosuppressive agents, and cytotoxic agents are the mainstay of therapy for many of the interstitial lung diseases

Patients with nonmuscular chest wall disorders and neuromuscular disease may develop problems with ventilation and gas exchange during sleep. The effect of decreased chest wall and lung compliance or decreased muscle strength is hypercapnia and hypoxemia, which occurs initially during sleep. Treatment of neuromuscular diseases includes preventive therapies to minimize the impact of impaired secretion clearance and the prevention and prompt treatment of respiratory infections. Treatment for massive obesity consists of weight loss, which causes dramatic improvement in pulmonary function test findings In advanced disease, when respiratory failure develops, these patients are treated with mechanical ventilation

CHRONIC BRONCHITIS (DIRTY CHEST)

LOBAR PNEUMONIA

PNEUMONIA WITH CONSOLIDATION

BILATERAL BRONCHOPNEUMONIA

PULMONARY ABSCESS

EMPHYSEMA