Asthma, COPD, bronchiolitis Flashcards
Day 2
Define asthma
Potential life threatening chronic respiratory disease if it is not well managed. Causes airway obstruction, bronchial hyperresponsiveness, airway inflammation, airway remodelling (hypertrophy of mucus gland, build up of scar tissue)
What are the 2 types of asthma ?
Extrinsic (atopic) - consequence of hypersensitive reactions associated with allergy ie pollen. Genetic predisposition for development of immunoglobin E - mediated response to common allergens.
Intrinsic (non atopic) - airway inflammation caused by infection, sudden exposure to cold, stress, smoking, NSAIDS
What are the main characteristics of asthma ?
Airflow limitation.
Airway hyperresponsiveness to stimuli or trigger factors → bronchospasm and contraction of the smooth muscle in the wall of the bronchi → narrowing of the airway and obstruction to breathing
Chronic inflammation → increased mucous production, swelling
Describe characteristics of chronic asthma
Chronic bronchoconstriction of the airway
Chronic bronchospasm of smooth muscle
Chronic production of mucous
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Chronic obstruction of air passage through the airways
What role do eosinophils play in asthma ?
release of harmful proteins and reactive oxygen species which damage the lining of the airways
Describe the pathophysiology of asthma
T-helper cells stimulated by allergen - atopic asthma
Stimulate cytokines and interleukin (inflammatory mediators)
This simulates B-cell response result in IgE antibody production
IgE antibodies bind with mast cells which are found in the airway resulting in inflammatory airway symptoms
Explain asthma exacerbation
Repeated exposure to allergen
Further release of IgE antibodies with mast cells
Release large amounts of histamine
Results in significant/worsening bronchospasm, bronchoconstriction and mucous production
Further worsened by the release of prostaglandins, leukotrienes, and cytokines
These stimulate the parasympathetic nervous system which causes smooth muscle contraction, further narrowing the airway
What is the pathophysiology of the characteristics of asthma ?
Airway swelling due to inflammation and fluid exudates – oedema
Increased mucous secretion → mucous plugs
Wheezing, cough, tight chest, breathlessness - Impaired gas exchanged – hypoxaemia, hypercapnia, acidosis (low blood pH) – stimulation of peripheral and central chemoreceptors leading to increase in respiratory rate and pulse
Define COPD
Chronic and recurrent obstruction of airflow in the pulmonary airways
Airflow obstruction usually is progressive and is accompanied by inflammatory responses to noxious particles and gases
What are the most common causes of COPD ?
Smoking, biomass fuel exposure, air pollution
What are risk factors for COPD ?
Genetic abnormalities (deficiency of antitrypsin)., abnormal lung development, accelerated aging, asthma and airway hyperresponsiveness
What are the 2 types of COPD ?
Emphysema and chronic bronchitis
Explain pathophysiology of emphysema
Chemical irritation of the alveoli walls (e.g.: smoking) causes damage to epithelial cells
Causes inflammatory and immune responses causing the alveolar walls to break down
Enlargement of airspaces in the bronchioles = decreased surface area for gas exchange
Loss of surfactant from walls also worsens effective gas exchange.
Explain pathophysiology of chronic bronchitis COPD
Damage to bronchus and bronchioles commonly caused by smoking. Cellular damage = inflammation = swelling and exudate:
Bronchoconstriction – limits airflow to lungs
Bronchospasm – limits airflow to lungs
Hypertrophy of goblet cells – increased mucous production and mucous plugs – limits airflow to lungs
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significant coughing, sputum production
What are the consequences of COPD ?
Destruction of alveoli wall leads to loss of elasticity of lung movement = easy to breathe in; but hard to breathe out
Enlarged alveoli spaces = air becomes ‘trapped’ resulting in hyperinflation – air remains within the lungs and isn’t breathed out
Hypoxaemia – low arterial oxygen levels - some patients can maintain normal oxygen levels by increasing respiratory effort
Hypercapnia - increased carbon dioxide levels - some patient’s - small percentage; in normal physiology carbon dioxide levels control our breathing; as disease progresses, patients with hypercapnia may loose sensitivity to carbon dioxide levels controlling breathing – hypoxic drive
What are the 2 types of acute respiratory failure ?
Type 1 hypoxaemic respiratory failure - failure of respiration (gas exchange function of the lung) leading to hypoxaemia with normal or low carbon dioxide levels
Type 2 hypercapnic/hypoxaemic respiratory failure – failure of ventilation leading to hypercapnia and hypoxaemia
What are the causes of ARF ?
Disorders of neuromuscular system Dysfunction of central nervous system
Disorders affecting chest wall and diaphragm
Airway abnormality
Pulmonary parenchymal diseases
What are the causes of RF in children ?
Upper airway obstruction (croup, tonsillitis)
Lower airway obstruction (asthma, bronch)
CNS fails to control ventilation
Mechanical impairment of ventilation
Failure to oxygenate tissues (hypovolaemia, septic shock, cardiac, metabolic disorders, intoxication)
What are the signs of hypoxaemia and hypercapnia ?
Hypox - cyanosis, confusion, fatigue, anxiety
Hyper - tachypnoea, headache, sweating
Signs of respiratory distress in children
Recession, nasal flaring, cyanosis, high HR and BP, tachypnoea. Normal artieral blood gas due to increasing respiratory efforts
What are the pre terminal signs of ARF ?
bradycardia, central cyanosis, oxygen <85% in air
What are physiological reasons for increased risk of respiratory compromise in children ?
Low lung volume, high metabolism, risk for apnoea, low efficiency of respiratory muscles
Define bronchiolitis
Constriction and blockage of the small airways due to the inflammatory response caused by the viral infection. Symptoms worsen 2-3 days after diagnosis
