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Respiratory Disorders

dr. Fajar Wahyu Pribadi


Overview
• Diagnostic Tests
• General Manifestations of Respiratory Disease
• Infectious Diseases
– Upper respiratory tract infections
• Common cold
• Sinusitis
– Lower respiratory tract infections
• RSV
• Pneumonia
• Obstructive Lung Diseases
– Lung Cancer
– Asthma
• Chronic Obstructive Pulmonary Disease (COPD)
– Emphysema
– Chronic Bronchitis
Diagnostic Tests
• Spirometry
• Arterial blood gas determination
• Oximeters
• Exercise tolerance
• Radiography
• Bronchoscopy
• Culture, sensitivity tests
General Manifestations of
Respiratory Disease
• Sneezing
• Coughing
– Irritation
– Controlled by medulla
– Constant, dry unproductive vs. productive cough
• Sputum
– Mucus discharge
– Yellowish-green
– Rusty, dark-colored
– Thick, sticky
– Hemoptysis
Manifestations
• Breathing patterns and characteristics
– Kussmaul respiration
– Labored respiration, prolonged inspiration/expiration
times
– Wheezing
– Stridors
• Breath sounds
– Rales
– Rhonchi
– Absence
Manifestations
• Dyspnea
– Severe
– Orthopnea
– Paroxysmal nocturnal dyspnea
• Cyanosis
• Pleural pain
• Friction rub
• Clubbed fingers
• Changes in ABG (arterial blood gases
– Hypoxemia  inadequate oxygen in blood
– Hypoxia  inadequate oxygen supply to cells
Causes of Hypoxia
• Low RBC, Hb
• Circulation impairment
• Excessive release of oxygen from RBC
• Impaired respiratory function
• CO poisoning
Upper Respiratory Tract Infections:
Common Cold (Infectious Rhinitis)
• Viral (rhinovirus)
• Spread thru respiratory droplets
• Highly contagious
• Initially mucous membranes of nose, pharynx
swollen, increased secretions
• Signs
– Nasal congestion and watery discharge
– Mouth breathing
– Change in tone of voice
– Sore throat, headache, slight fever
– Cough
Common Cold
• Infection, inflammation can spread
– Laryngitis
– Bronchitis
• Treatment is symptomatic
– Acetaminophen
– Decongestant
– Antihistamine
– Humidifiers
– Are antibiotics prescribed?
Secondary Bacterial Infections
Sinusitis
• Secondary bacterial infection
• Obstruct drainage in 1 or more paranasal sinuses
• Common causative organisms
– Pneumococci
– Streptococci
– Haemophilus influenzae
• Exudate accumulates
• Signs
– Nasal congestion, fever, sore throat
• Diagnosis confirmed by radiograph, transillumination
• Decongestants, analgesics
• Antibiotics
Lower Respiratory Tract Infections:
Bronchiolitis (RSV Infection)
• 2-12 month
• Caused by syncytial virus
• Transmitted by oral droplet
• Predisposing factors (asthma, smoking)
• Causes necrosis and inflammation of small bronchi and bronchioles
• Signs
– Wheezing and dyspnea
– Rapid, shallow respirations
– Cough
– Rales
– Chest retractions
– Fever
• Treatment
– Supportive and symptomatic
Pneumonia
• Primary acute or secondary
• Risk following aspiration, inflammation in
lung
• Transmission
– Inhaling virus
– Resident bacteria spreading along mucosa
– Aspiration in secretions
Classification of the Pneumonias
• Causative agent
– Virus, bacteria, fungus
– Lobar is typically bacterial
• Pneumococcus
• Anatomical distribution of lesion
– Both lungs or lobar
• Pathophysiologic changes
– Viral  changes in interstitial tissue or alveolar septae
– Pneumococcal  alveoli inflamed and fluid filled
• Exudate
• Epidemiologic categories
– Nosocomial
– Community acquired
Lobar Pneumonia
• Streptococcal
pneumoniae,
pneumococcal
• Infection localized in 1
or more lobes
Stages of Pneumonia
• Congestion
– Inflammation and vascular congestion in alveolar wall
• Exudate forms in alveoli
– Interferes with oxygen diffusion

• Consolidation
– Neutrophils, RBCs, fibrin accum in exudate
• Form solid mass
• RBCs break down, infection resolves
– Macrophages break down exudate
• Expectorated or resorbed
Consolidation
Pneumonia
• Pleurae typically involved
– Infection in pleural cavity
• Emphysema
– Adhesions between membranes
• Manifestations
– Sudden onset
– Systemic signs: high fever, chills, fatigue
– Dyspnea, tachycardia
– Pleuritic pain
– Rales
– Productive cough
Pneumonia
• Treatment
– Antibacterials (Penicillin)
– Supportive measures
– Pneumococcal vaccine
Obstructive Lung Disease:
Lung Cancer
• Primary or secondary; benign rare
– Primary is major cause of death
• Linked with cigarette smoking
• Metastases develop freq in lung b/c:
– Venous return and lymph vessels bring tumor
cells from distant site in body  heart  lung
• Poor prognosis
Normal Lung vs. Cancerous Lung
Normal Lung vs. Cancerous Lung
Types of Lung Cancer
• Bronchogenic carcinoma
– Most common
– Arise from bronchial epithelium
• Squamous cell carcinoma
– Develop from epithelial lining in bronchus
– Project into airway
• Adenocarcinomas and bronchoalveolar cell carcinoma
– Found on lung periphery
– Less symptomatic, more difficult to treat
• Small cell carcinoma
– Rapidly growing; located near major bronchus
– Invasive and metastize early in dev
• Large cell carcinoma
– Found in periphery
– Consist of large, undifferentiated cells
– Rapid growth rate, metastize early
Bronchogenic Carcinoma
Lung Cancer—Pathophysiology
• First change
– Metaplasia, change in epithelial tissue
• Smoking, chronic irritation
• Reversible if irritation removed
– Loss of ciliated pseudostratified epithelium
• More vulnerable to irritants
• Next
– Dysplasia, carcinoma develop
– Hard to detect
Lung Cancer—Effects of Tumors
• Obstruction of air flow
• Inflammation
• Pleural effusion, hemothorax,
pneumothorax
• Paraneoplastic syndrome
Lung Cancer—Etiology
• General stats
– 173,330 new cases each year
– 160,440 deaths per year
• Smoking (primary and secondary)
– 87% of lung cancers related to smoking
– 1 out of 10 chances of developing lung cancer
• Maybe a genetic factor
• Occupational exposure to carcinogens
• Irritant that leads to chronic inflammation
– Cause cell changes
• Smoking: ciliated columnar  squamous
Lung Cancer—Signs and
Symptoms
• Insidious onset
• Normally metastized before diagnosis
• 4 possible categories of signs of lung
cancer
– Direct effects of tumor
– Systemic effects of cancer
– Paraneoplastic syndromes
– Metastizes at other sites
Lung Cancer—Early Signs (#1)
• Persistent, productive cough, dyspnea,
wheezing
• Detection on chest X-ray
• Hemoptysis
• Pleural involvement
• Chest pain
• Hoarseness
• Facial, arm edema; headaches
• Dysphagia
Lung Cancer (#2-4)
• Systemic signs
– Wt. loss, anemia, fatigue
• Paraneoplastic syndrome
– Signs of endocrine disorder
– Depends on hormone being secreted
• Signs of metastasis depends on site
Lung Cancer—Diagnostic Tests
• Chest X-rays
• Bronchoscopy
• Pulmonary function tests
Lung Cancer—Treatment
• Surgery on localized lesions
• Chemotherapy and radiation
• Poor prognosis unless tumor in early
stages of development
Asthma
• Periodic episodes of severe but reversible
bronchial obstruction
• Frequency may lead to irreversible damage and
COPD
• 2 types
– Extrinsic asthma
• Acute episodes triggered by type I hypersensitivities
• Onset in childhood
– Intrinsic asthma
• Onset during adulthood
• Stimuli target hyperresponsive tissue = acute attack
Asthma—Pathophysiology:
Acute Attack
• Both types
• Bronchi and bronchioles respond to stimulus
with 3 changes
– Bronchoconstriction
– Inflammation of mucosa with edema
– Increased secretion of thick mucus in passageways
• Changes may result in partial or total obstruction
of airways
– Interferes with oxygen supply, air flow
Asthma—Pathophysiology:
Extrinsic Asthma
• 1st stage
– Allergen reacts with IgE on previously sensitized mast
cells in resp. mucosa
• Release chemical mediators (histamine, prostaglandin)
– Stimulates vagus nerve
• Reflex bronchoconstriction
• 2nd stage
– Hours later
– Increased leukocytes release more chemical
mediators
• Prolong bronchoconst and epithelial damage
• Increase WBC
– Obstruction, hypoxia
Asthma—Pathophysiology:
Partial Obstruction
• Small bronchi, bronchioles
• Air trapping with hyperinflation of lungs
• Air only partially expired
• Expiration passive
– Now less force to move air out
– Forced collapses bronchial wall
• Even more difficult to expire
• Increased residual volume
– More difficult to inspire fresh air, cough
Asthma—Pathophysiology:
Total Obstruction
• Mucus plugs completely block
• Air in distal section diffuses out
– Cannot be replaced
• Lung in that section collapses
• Both (partial and total) lead to hypoxia and hypoxemia
• Status asthmaticus
– Persisant severe asthma attack
– Does not respond to therapy
– Can be fatal
• Chronic asthma and COPD may develop
– Irreversible damage in lungs
Asthma—Etiology
• Family history of hay fever, asthma,
eczema
• Significant rise due to:
– Sedentary lifestyles and obesity
– Increased time indoors
– Increased air pollution
Asthma—Signs and Symptoms
• Cough, dyspnea, tight feeling in chest
• Wheezing
• Rapid, labored breathing
• Thick, sticky mucus coughed up
• Tachycardia and pulse paradoxus
– Pulse differs on inspiration and expiration
• Hypoxia
• Respiratory acidosis
• Severe respiratory distress
• Respiratory failure
Asthma—Treatment
• General measures
– Determine allergies
– Avoid triggers
• Acute attacks
– Inhalers
• Bronchodilators (albuterol)
• Most effective at 1st indication of attack
– Controlled breathing techniques and decrease anxiety
– Glucocorticoids
• Hospital care—status asthmaticus
• Prophylaxis and treatment of chronic asthma
– Leukotrine receptor antagonists (Singulair)
• Block inflammation response
• Taken regularly, not effective for acute attacks
– Cromolyn sodium
• Inhibits release of chemical mediators from sensitized mast cells
• Not effective for acute attacks
Chronic Obstructive Pulmonary
Disease (COPD)
• Progressive tissue damage and obstruction of
airways
• Affect individual’s ability to work and function
indep
– Eventual resp failure
• Leads to R CHF
• Includes
– Emphysema
– Chronic bronchitis
– Asthma
Emphysema—Pathophysiology
• Significant change is destruction of
alveolar walls and spaces
– Leads to lg, inflated alveoli
• Classified by specific location of changes
– Ex: Distal alveoli emphysema
– Ex: Bronchiolar emphysema
Emphysema—Pathophysiology:
Contributing Factors
• Genetic
– Low alpha1-antitrypsin
• Protein normally present in tissues
• Inhibits action of proteases
– Destruction of enzymes released by neutrophils during
inflammation
– Ex: Elastase
» Breaks down elastic fibers
» Destructive process increases in people with low alpha1-
antitrypsin
• Smoking
– Increases # neutrophils in alveoli and release of
elastase
– Decreases effects of alpha1-antityrpsin
Emphysema—Pathophysiology:
Effects of Tissue Changes on Lung
Function
• Break down of alveolar wall
– Decrease SA for gas exchange
– Loss of pulmonary capillaries
– Loss of elastic fibers
– Altered ventialtion-perfusion ratio
– Decreased support for small bronchi
• Fibrosis and thickening of bronchial wall
• Progressive difficulty with expiration
– Air trapping, increased residual volume
– Overinflation of lungs
– Fixation of ribs in inspiration position
Severe Emphysema
• Adjacent damaged alveoli
• Lung appears full of holes
• Frequent infection
• Lg. belbs near lung
surface
– May rupture
• Pneumothorax
• Pulmonary hypertension
or R CHF
Emphysema—Etiology
• Cigarette smokers
• Genetic
• Exposure to air pollutants
• Conjunction with other chronic lung
disorders
– Cystic fibrosis
– Chronic bronchitis
Emphysema—Signs and
Symptoms
• Onset insidious
• Dyspnea occurs 1st on exertion
• Hyperventilation with prolonged expiration
– Use of accessory muscles, hyperinflation
– “barrel chest”
• Anorexia, fatigue
• Clubbed fingers
Emphysema—Diagonstic Tests
• Chest X-rays
• Pulmonary function tests
– Indicate presence of increased residual
volume and total lung capacity
– Decreased forced expiration volume and vital
capacity
Emphysema—Treatment
• Avoid resp infections, irritants
• Stop smoking
• Pulmonary rehabilitation
• Appropriate breathing techniques
• Maintain adequate nutrition, hydration
• Bronchodilators, antibiotics, oxygen therapy
– As condition advances
• Lung reduction surgery
– Remove part of lung
Chronic Bronchitis—
Pathophysiology
• Significant changes in bronchi
– Irreversible and progressive
• Inflammation, obstruction, repeated infection, chronic coughing
• Inflamed, swollen mucosa
• Hypertrophy/plasia of mucus glands
– Increased secretions (increased # goblet cells)
– Decreased ciliated epithelia
• Fibrosis and thickening of bronchial wall
– Further obstruction; pooling of secretions
• Decreased oxygen
– Cyanosis during cough
• Severe dyspnea and fatigue
• Pulmonary hypertension and R CHF
Chronic Bronchitis—Etiology
• Smoking
– Crap! Not again!
• Living in urban areas
• Living in industrial areas
Chronic Bronchitis—Signs and
Symptoms
• Constant productive cough
• Tachypnea, shortness of breath
• Thick, purulent secretions
• Severe cough and rhonchi
• Airway obstruction
– Hypoxia, cyanosis
• R CHF, pulmonary hypertension
Chronic Bronchitis—Treatment
• Decrease exposure to irritants
• Expectorants, bronchodilators, chest
therapy (postural drainage)
– Remove excess drainage

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