Respiratory Disorders

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Name:_________________________________________
General Medicine
Respiratory Disorders
Lecture Notes
Learning Objectives:
Identify common manifestation of
respiratory diseases: like
Pneumonias, bronchopneumonia,
bronchial Asthma.
-Describe their classification,
aetiology, clinical manifestations,
investigations & treatment.
- List the causes of dysnea, acute
chest pain & haemoptysis
Dr. J. Satish Kumar, MD, Department of Basic & Medical Sciences, AUST
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
Components of the Respiratory System
Figure 23–1
Diagnostic Tests
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Spirometry
Arterial blood gas determination
Oximeters
Exercise tolerance
Radiography
Bronchoscopy
Culture sensitivity tests
General Manifestations of Respiratory
Disease
• Coughing
– Irritation
– Controlled by medulla
– Constant, dry unproductive vs. productive cough
• Sputum
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Mucus discharge
Yellowish-green
Rusty, dark-colored
Thick, sticky
• Hemoptysis
• Dyspnea
• Chest Pain
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
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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
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Low RBC, Hb
Circulation impairment
Excessive release of oxygen from RBC
Impaired respiratory function
CO poisoning
Upper Respiratory Tract Infections:
Common Cold (Infectious Rhinitis)
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Viral (rhinovirus)
Spread thru respiratory droplets
Highly contagious
Initially mucous membranes of nose, pharynx
swollen, increased secretions
• Signs
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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
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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
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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
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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
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
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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
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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
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Hypoxia
Respiratory acidosis
Severe respiratory distress
Respiratory failure
Asthma—Treatment
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General measures
– Determine allergies
– Avoid triggers
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Acute attacks
– Inhalers
• Bronchodilators (albuterol)
• Most effective at 1st indication of attack
– Controlled breathing techniques and decrease anxiety
– Glucocorticoids
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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
Alveolar Organization
Figure 23–11
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 alpha1antitrypsin
• 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
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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
COPDEmphysema
Severe Emphysema
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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
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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
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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
• Living in urban areas
• Living in industrial areas
Chronic Bronchitis—Signs and Symptoms
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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
Dental Treatment Considerations
for Asthmatics
- avoid known triggers (stress, allergens,
chemical irritants)
- advise patient to continue taking usual
medications
- advise patient to bring inhalers to
appointment
- avoid elective treatments during upper
respiratory infections when symptoms are
poorly controlled
- avoid use of aspirin and NSAIDS
- watch sulfiting agents in LA with
vasoconstrictor = bronchoconstriction
- avoid erythromycin with theophylline = toxicity
reaction
- supplemental adrenal therapy with extreme
stress in long-term steroid users
Dental Treatment Considerations
for Patients with COPD
- promote smoking cessation
- watch for wheezing, orthopnea while
recumbent
- activate EMS for acute respiratory
distress
- avoid sedatives
- if severe COPD, risk for developing pulmonary
hypertension, increasing risk for cardiac
arrhythmias = avoid stress
- adrenal supplementation may be necessary for
patients taking long term steroids if procedure
is likely to produce severe stress
- oxygen (versus CO2) becomes drive for
ventilation: if given too much oxygen, may
induce apnea/acute respiratory failure
- limit oxygen to less than 3L/minute, or deliver
by nasal cannula during stressful/painful
dental procedures
- promote vaccination against influenza
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