Obstructive Airway Disease Flashcards
Overview of Obstructive Airway Disease
Disease of the airways (bronchi and larger bronchioles) causing the trapping of air within the lungs
Usually associated with inflamed, and easily collapsible airways
Includes: asthma, COPD (chronic bronchitis and emphysema), and bronchiectasis
Definition of Asthma
Chronic inflammatory condition concerning the airways which is associated with acute reversible exacerbations which in turn are characterised by smooth muscle spasm in the bronchi and bronchioles
These exacerbations are usually triggered by something
Asthma Triggers
Exercise, cold air, pollutants (Ozone, sulphur dioxide, cigarette smoke), drugs (NSAIDs, Beta blockers), emotion, allergens (dust mites, grass pollen, pets)
Occupational triggers come in 2 flavours: low molecular weight (colophony fumes, wood dust) which react with epithelium and are non-IgE related, and high molecular weight (latex, antibiotics) which involve specific IgE
Prevalence of Asthma
Thought to affect 15% of the global population
Rates are higher in developed countries (Western Europe) with rates far lower in Far Eastern countries (China, Malaysia) and Eastern Europe
Interleukin-4 and Asthma
Release of IL-4 from Th2 cells stimulates the production of IgE ntibodies which in turn coats mast cells, triggering the release granules containing histamines, leukotrienes and prostaglandins
The release of IgE makes this a type 1 hypersensitivity reaction
Interleukin-5 and Asthma
Release of IL-5 (& IL-13) from Th2 cells activates eosinophils which in turn release cytokines and leukotrines
Th2 Cells and Asthma
Dendritic cells phagocytose allergens in airways and present these to CD4 T cells, these T cells differentiate into Th2 cells which lead the allergic response
Histology/pathophysiology of Asthma
Bronchial inflammation characterised by T lymphocytes, mast cells, eosinophils +associated plasma exudation, oedema, smooth muscle hypertrophy, matrix deposition, mucus plugging, and epithelial damage
Atopy
Defined as the genetic tendency to develop allergic diseases (hay fever, asthma) in response to common allergens
Runs in families
Characterised by wheeling skin reactions to allergen
Found to have circulating allergen specific IgE
Results of Chronic Airway Inflammation in Asthma
The exacerbations of airway hyper-responsiveness (broncho constriction) increase in severity and occurrence with each trigger
Airway remodelling may occur in sever cases, characterised by smooth muscle hypertrophy, collagen deposition, and basement membrane thickening, resulting in a fixed airway obstruction
Chronic activation of epithelium leads to loss of cilla and makes patients more susceptible to common infections (exhaled NO can be measured to detect inflammation)
Bronchial Challenge Test
Patients inhale increasing methacholine and histamine whilst measuring FEV1
In asthmatic patients, this will cause transient airway obstruction (decrease of about 20% in FEV1 is the standard measure)
Record at what conc. standard obstruction occurs
Obstruction may occur at HIGH doses in patients with seasonal wheeze (pollen season), allergic rhinitis, very low grade asthma, and patients with no reported respiratory symptoms
Blood tests for me
Stool culture = neg.
C diff. = neg
H.pylori = neg
Peak Inspiratory Flow Rate in Asthma
A measure of the peak rate of flow on forceful expiration
Reduced in asthmatic patients (~25%-60% less than predicted value)
Spirometry in Asthma
Obstructive pattern will be present
Characterised by a preserved FVC, decreased FEV1 (0.8 of predicted), FEV1/FVC is less than 0.7
CXR in Asthma
Usually normal, but may exhibit hyperinflation
Presentation of Asthma
Intermittent shortness of breath, intermittent wheeze, dry or productive cough
Any associated triggers?
Nocturnal cough (children)/night wakening with SOB
Recent changes?
Impact upon life?
Management of Acute Asthma Attack
Oxygen Salbutamol Hydrocortisone IV acces + Ipratropium Theophylline Magnesium sulphate Escalate care
Evaluating an Acute Asthma Attack
Life threatening = 33 (PEFR value is less than that percent of predicted), 92 (oxygen salts are less than), C(yanosis), H(ypotension), E(xhaustion), S(ilent chest), the T(achycardia)
Severe = PEFR<50%, cant complete sentences, RR>24, PR>110
Moderate = PEFR<75%
Mild>75%
Management of Intermittent Asthma
Lifestyle advice: avoid triggers, quit smoking
Pharmacological: Salbutamol (SABA) when required
Follow up: every 12 months, progress to chronic pathway if one of the following is true: 1. Asthma attack in the past year 2. Symptomatic 3 or more times per week 3. Using inhaler 3 or more times per week 4. Waking up at night once a week
Management of Chronic Asthma: Lifestyle Advice and Education
Identify and avoid triggers, smoking cessation
Teach and witness proper inhaler technique
Encourage recording of peak flow and symptom diary
Inform patients the function of and when to use each inhaler
Aims of Treating Asthma
Abolish symptoms Restore or achieve best possible lung function Reduce risk of severe attacks Facilitate normal growth Minimise impact on life
Pharmacological Treatment of Chronic Asthma
Escalation Pathway
To begin with daily symptoms + <80% PEFR is treated with inhaled corticosteroids (beclamethasone) along with PNR SABA (salbutamol)
If still not controlled add the use of a LABA (salmetarol), asses response, if inadequate increase steroid dose
If poor control persists trial large dose steroids, leukotriene receptor antagonist, oral theophylline, or B2 selective beta blockers
If response still poor add daily oral steroid tablet (prednisolone)
Alternative Pharmacological Treatments for Asthma
Non-escalation pathway
Antimuscarinic agents (SAMA for acute episodes and LAMA for chronic) Sodium cromoglycate (& nedocromil glycate) works for mild asthma but is no longer favoured Methotrexate may be used as a steroid sparing agent Monoclonal antibodies (omulizab) works for patients who require frequent hospitalisations
Prognosis of Asthma
Childhood asthma tends to resolve in teens and reappear in the second, third, fourth decades
Progression of disease may still occur without noticeable symptoms so it is important to treat with preventative therapies from an early diagnosis
Deterioration sped up by airway remodelling
Definition of COPD
A disease state characterised by airflow limitation that is not fully reversible.This limitation is usually progressive and associated with a hyper responsiveness to noxious fumes/particulates
Overarching diagnosis accounting for chronic bronchitis, emphysema, and other diseases that come with airflow obstruction and parenchyma destruction
Associated with a number of other inflammatory diseases (ischaemic heart disease, hypertension, diabetes…), suggesting a generalised response
Aetiology of COPD
90% of COPD cases can be linked to long-term inhalation of cigarette smoke, although only 10-20% of heavy smokers develop COPD (genetics?)
Other causes include inhalation of biofuel smoke, cooking in poorly ventilated areas
Risk of developing COPD increase with lower socioeconomic class, urban living, increased pollution
Chronic Bronchitis Pathophysiology
Most common finding is increased numbers of goblet cells in the larger bronchi, inflammation also leads to increased mucus secretion
Characterised by neutrophilic inflammation and CD8 infiltrate
Epithelia may be ulcerated and metaplasia from squamous to columnar may occur, later, fibrosis may lead to narrowing of the lumen
Smooth muscle spasm and hypertrophy may occur
Low grade inflammation is reversible, fibrosis of airway leads to irreversibility
Defined as productive on most days for more than 3/12 for two consecutive years
Emphysema Pathophysiology
Abnormal, permanent enlargement of airspaces distal to the terminal bronchiole with destruction of their walls accompanied by no obvious fibrosis, thought to be secondary to small airway inflammation
Varieties of Emphysema
Centri-acinar = distension and damage of lung tissue surrounding respiratory bronchioles, whilst alveoli are preserved. Most common, only severe disease is associated with disability
Pan-acinar = associated with alpha-1 antitrypsin deficiency. Distension and destruction across the whole acinus. Associated with severe V/Q mismatch, and severe airflow limitation
Irregular and pareseptal also exists
Alpha-1 antitrypsin deficiency
Alpha-1 antitrypsin is a proteinase inhibitor which is secreted by the liver into the blood stream
In the lung, it prevents the actions of neutrophil elastase (breaks down connective tissue of the alveolar wall)
Deficiency is homozygous genetic (but a genetic presence does not always mean chest symptoms)
Associated with SOB under the age of 40 +/- Hx smoking, radio graphic evidence of basal emphysema
Pink Puffer
Most associated with emphysema dominant COPD, CO2 PaCO2 is not greatly effected by V/Q mismatch and CO2 conc. may even be lower than normal due to increased alveolar ventilation
Characterised by dyspnea, minimal cough, increased RR, flush skin, pursed-lip breathing, accessory muscle use, cachexia (muscle wastage), barrel chest, decreased breath sounds
Complications include pneumothorax and weight loss
Blue Bloater
Most associated with chronic bronchitis dominant COPD, failure to maintain respiratory effort leads to a chronic increase in PaCO2, desensitising the body to it, and only rely on hypoxaemia driven ventilation.
Characterised by chronic productive cough, purulent sputum, haemoptysis, mild dyspnea, cyanosis, peripheral oedema (cor pulmonale) crackles/wheeze, prolonged expiration, fluid retention (renal hypoxia)
Complications include polycythemia and pulmonary hypertension
Presentation of COPD
Hx of smoking/job involving irritants
Progressively worsening SOB accompanied by cough producing grey/white sputum
Symptoms worse in cold/damp environment or in response to pollution
Colds seem to ‘settle’ in the chest, frequent infective exacerbations
Respiratory Failure
Type 1 = PaO2 <8kPa (60mmHg)
Presents with dyspnea, confusion, tachycardia, cyanosis, tachypnoea
Causes include pulmonary oedema, COPD, asthma, pneumonia, ARDS, PE
Type 2 = PaCO2 >7pKa (53mmHg) +/- PaO2 <8kPa (60mmHg)
Presents with headache, change of behaviour, coma, papilloedema, warm extremities
Most commonly caused by COPD, but may also be seen in mechanical or CNS issues
Cor Pulmonale or Pulmonary Hypertension
Abnormal enlargement of the right side of the heart as a result of disease of the lungs or pulmonary blood vessels leading to increased pulmonary pressure
Hypoxic kidney leads to fluid retention (and therefore peripheral oedema)
Presents initially with a parasternal heave and a loud pulmonary second sound
As disease progresses, severe fluid overload may cause tricuspid incompetence alongside a greatly elevated JVP, ascites, and liver swelling
Spirometry in COPD
FEV1/FVC = decreased (<75%)
FEV1 is less than predicted (mild = >80%, moderate = 50-79%, severe = 30-49%, V. Severe = <30%)
Obstruction may be partly reversed in the application of a SABA, as such it may be difficult to distinguish COPD from asthma
DCLO may be low in the presence of emphysema
CXR in COPD
Often normal (even in advanced disease)
Overinflation and a flattened diaphragm are common findings
Large bullae may be seen in emphysema patients
Peripheral vessels may be ‘pruned’
ABG in COPD
Often normal at rest
However upon exercise hypoxia +/- hypercapnia may be present
General Treatment of COPD
SMOKING CESSATION is the most effective treatment, prolonging life and reducing morbidity
Encourage exercise
Flu vaccine to prevent exacerbations
Pulmonary physiotherapy
Nutritional advice (increase/decrease weight)
Pharmacological Escalation Pathway for COPD
If mild symptoms are present begin with either a SABA (salbutamol) or SAMA (ipratropium) taken every 4-6 hours (or PRN)
If moderate symptoms are present but FEV1>50% add a LABA (salmeterol) or LAMA (triotropium), however, if FEV1<50% add an inhaled corticosteroid (beclamethasone), long-acting theophylline may also be considered
If severe symptoms are present oral steroids (prednisolone) may be added
If pulmonary hypertension is present, long term oxygen therapy is indicated
Other Pharmacological Considerations in COPD
Antibiotics to be kept at home to be taken when the sputum turns yellow/green
Phosphodiesterase-4 (roflumilast) inhibitors may be given alongside bronchodilators
Antimucolytic agents may be given to reduce sputum viscosity
Diuretic therapy may be used in oedematous patients
Nocturnal Hypoxaemia
Occurs due to inhibition of accessory muscles during REM, shallowed breathing during REM, and increased upper airway resistance
Increases pulmonary pressure and polycythaemia
Episodes usually end with the sudden awakening of the patient
Managed by nocturnal administration of oxygen and ventilation support
Surgical Treatment of COPD
Surgical bullectomy can re-expand a collapsed lung
Certain patients may receive lung reduction to increases elastic recoil leading to decreased obstruction and increases diaphragm efficiency
Single lung transplant is beneficial but does not increase mortality
Acute Exacerbation of COPD
Usually presents in winter as a result of bacterial infection (not necessarily)
Presents with worsened SOB/wheezing/cough and decreased exercise tolerance
Take a sputum culture
Managed by O2 (24% Venturi) with a target of 88-92%, nebulised salbutamol and ipratropium, steroids (IV hydrocortisone or oral prednisolone) and amoxicillin if infection suspected
Asthma Vs. COPD
Early onset Vs. Late onset
Smoking unrelated Vs. Smoking related
Episodic symptoms Vs. Chronic continual symptoms
Diurnal variation Vs. No diurnal variation
Non-productive cough Vs. Productive cough
Reversible Vs. Non-reversible
Preserved FVC/gas exchange Vs. Reduced FVC/gas exchange
Eosinophilic inflammation Vs. Neutrophilic inflammation
