L18 Asthma and COPD Flashcards
Risk factors of asthma?
Signs/Symptoms of Asthma
Symptoms of Asthma: Cough, Wheeze, Shortness of Breath, Chest Tightness
Signs of Asthma: Hyperexpansion of chest cavity, prolonged expiratory time, expiratory wheezing, use of respiratory muscles
What allows asthma to be differentiated from COPD?
Asthma’s reversibility w/ broncho dilator allows it to be differentiated from COPD
What is Atopy and what is its significance?
Atopy is the tendency to produce an exaggerated immunoglobulin E immune response to otherwise harmless substances in the environment
- Presence of atopy makes asthma more likely than COPD
- Determines sensitivity to indoor allergens
- Serologic testing:
– IgE- elevations indicate the presence of allergic sensitization
– radioallergosorbent test (RAST)
• Allergen skin testing– Guides interventions to reduce exposure
Pathology of Asthma?
Reduction in airway luminal diameter
- excessive mucus production
- thick basement membrane
- airway inflammation
- bronchial hyper-responsiveness
Interactions between CD4 T Cells and B Cells => IgE Synthesis
Airway obstruction caused by some combination of
– Airway smooth-muscle constriction
– Inflammation of the bronchi
– Abnormal smooth-muscle contractility or Excess smooth-muscle mass
– Eosinophil influx
Th1 versus Th2 Phenotype of Asthma?
Asthma Treatment?
Reduction in bronchial inflammation when treated => still too many goblet cells
relaxation of airway smooth muscle (bronchodilators)
suppression of airway inflammation (anti-inflammatory drugs)
newer medication (dual effects)
– leukotriene modifiers
– Anti IgE therapy
drug combinations– inhaled corticosteroids combined with long-acting β-adrenergic agonists
Characteristics of COPD?
COPD is Chronic airflow obstruction due to chronic bronchitis and/or pulmonary emphysema
Primarily caused by cigarette smoking
Some patients with asthma develop poorly reversible airflow limitation
– indistinguishable from patients with COPD
– for practical purposes are treated as asthma
Diagnosis of COPD?
Diagnosis of COPD considered in any patient who has the following symptoms:
– cough
– sputum production or
– dyspnoea or
– history of exposure to risk factors for the disease (tobacco smoking++)
The diagnosis is confirmed with spirometry
Assessment of COPD severity
– spirometry
– functional dyspnoea
– body mass index = weight (Kg)/ height2 (m)
COPD Pathology? (4 Compartements impacted)
COPD => pathological changes in 4 different compartments of the lungs:
- central airways
- peripheral airways
- lung parenchyma
- pulmonary vasculature
Physiological Abnormalities in COPD
Physiological abnormalities in COPD
– mucous hypersecretion
– ciliary dysfunction
– airflow limitation
– hyperinflation
– gas exchange abnormalities
– pulmonary hypertension: destroys capillary beds => secondary hypertension from increased PVR
Smoking’s Contribution to COPD
Smoking is the main risk factor for COPD + Other inhaled noxious particles and gases
Oxidative stress from free radicals in tobacco smoke => Imbalance of proteinases and anti-proteinases in the lungs
– Free radicals impair activity of anti-proteases
– ⇑ Proteases enzymes damages the lungs
Inflammatory response in the lungs
Irritation of the mucous membrane
– bronchitis
– Increased mucous secretion
– ball and valve obstruction
Chornic Bronchitis Pathogeneis?
known as “blue bloaters”
bronchi inflammation => eventual fibrosis/scarring
Pathogenesis
• inflammation of the wall of bronchi and bronchioles
• increased mass of mucous glands=> excessive production of mucus and sputum
• Airways become narrowed => ⇓ airflow
Clinical Diagnostic Criteria fro Chornic Bronchitis
Cough + sputum (productive cough) for 3 months/year over 2 years
Complications of Chronic Bronchitis?
Hypercapnia
Respiratory acidosis
Hypoxemia
Polycythemia (elevated hemoglobin levels)
CO2 retention
=> pulmonary artery vasoconstriction
=> pulmonary hypertension
=> cor pulmonale
=> right heart failure
Emphysema Pathogenesis
pink puffer
Alveoli (air sacs) enlargement and destruction => minimal inflammation, some fibrosis
Pathogenesis
Destruction of lung tissue distal to the terminal bronchiole (acinus) => permanent enlargement of the air spaces
Destruction of the alveolar walls
=> destruction of the capillary bed
=> increased pulmonary vascular resistance
=> pulmonary hypertension
Increased Lung compliance => Reduced elasticity, Hyperinflation, Poor lung mechanics
What is the role of Alpha-1 Anti Trypsin Deficiency?
What do people w/o it develop?
What can cure it?
Alpha 1 Antitrypsin (AAT) is a protease inhibitor “lung protector” produced by liver and immune cells
In absence of ATT => neutrophil elastase not inhibited
=> unregulated breakdown of elastin
=> increased alveolar compliance
In the absence of AAT, patients develop: emphysema (PANACINAR) and liver cirrhosis
Liver transplantation can cure the condition if diagnosed in childhood
Two Types of Emphysema?
Centrilobular (most common)
– damage is limited to the central part of the lobule or acinus (upper lobes most affected)
– preserved peripheral alveolar ducts and alveoli
– Smokers
Panacinar (rare)
– destruction of the entire lobule
– Genetic: Alpha-1-anti-trypsin deficiency (protease inhibitor) =>increased destruction of elastin
– IVDU: can be seen in talc IV drug abuse and in Ritalin use
Clinical Signs of Emphysema (3)
Barrel-shaped chest
– increased antro-posterior diameter
– sternum pushed forward
– widened subcostal angle
Accessory muscles of respirations
– hyperactive
– prominent (e.g.,sternomastoids) (gasping for breath)
Intercostal spaces
– widened
– Horizontal ribs
Complications of COPD?
Emphesema vs. Bronchtis?
Infection
– Pneumonia
– bronchiectasis
– tuberculosis (due to decreased local immunity of the lung)
Pulmonary hypertension
– in bronchitis
• fibrosis involving lung capillaries.
– in emphysema
- destruction of capillary beds in alveolar walls
- compression of the alveolar septa by trapped air
Pneumothorax
– rupture of bullae into the pleura
– air in the pleural cavity
– push the lung towards the mediastinum
– lung collapse with mediastinal
COPD Causes of Death?
COPD Causes of Death
Respiratory failure: ventilation, perfusion, and diffusion are all affected with resultant severe hypoxaemia and hypercapnia
Core pulmonale: Right-sided heart failure due to pulmonary hypertension induced by lung lesion
Lung cancer: squamous metaplasia (chronic bronchitis) & smoking are risk factors for lung cancer
Management of COPD?
Established COPD is not curable but controllable
Smoking cessation -Most important factor in slowing down the progression of COPD
Pharmacotherapy
Bronchodilators: β2 agonists, M3 antimuscarinics, leukotriene antagonists
=> relax the smooth muscles of the airway allowing for improved airflow
