Obstructive Airway Disease

Question 1

Overview of Obstructive Airway Disease

Answer 1

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

Question 2

Definition of Asthma

Answer 2

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

Question 3

Asthma Triggers

Answer 3

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

Question 4

Prevalence of Asthma

Answer 4

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

Question 5

Interleukin-4 and Asthma

Answer 5

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

Question 6

Interleukin-5 and Asthma

Answer 6

Release of IL-5 (& IL-13) from Th2 cells activates eosinophils which in turn release cytokines and leukotrines

Question 7

Th2 Cells and Asthma

Answer 7

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

Question 8

Histology/pathophysiology of Asthma

Answer 8

Bronchial inflammation characterised by T lymphocytes, mast cells, eosinophils +associated plasma exudation, oedema, smooth muscle hypertrophy, matrix deposition, mucus plugging, and epithelial damage

Question 9

Atopy

Answer 9

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

Question 10

Results of Chronic Airway Inflammation in Asthma

Answer 10

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)

Question 11

Bronchial Challenge Test

Answer 11

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

Question 12

Blood tests for me

Answer 12

Stool culture = neg.
C diff. = neg
H.pylori = neg

Question 13

Peak Inspiratory Flow Rate in Asthma

Answer 13

A measure of the peak rate of flow on forceful expiration

Reduced in asthmatic patients (~25%-60% less than predicted value)

Question 14

Spirometry in Asthma

Answer 14

Obstructive pattern will be present

Characterised by a preserved FVC, decreased FEV1 (0.8 of predicted), FEV1/FVC is less than 0.7

Question 15

CXR in Asthma

Answer 15

Usually normal, but may exhibit hyperinflation

Question 16

Presentation of Asthma

Answer 16

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?

Question 17

Management of Acute Asthma Attack

Answer 17

Oxygen 
Salbutamol
Hydrocortisone 
IV acces + Ipratropium
Theophylline 
Magnesium sulphate
Escalate care

Question 18

Evaluating an Acute Asthma Attack

Answer 18

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%

Question 19

Management of Intermittent Asthma

Answer 19

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

Question 20

Management of Chronic Asthma: Lifestyle Advice and Education

Answer 20

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

Question 21

Aims of Treating Asthma

Answer 21

Abolish symptoms
Restore or achieve best possible lung function
Reduce risk of severe attacks
Facilitate normal growth
Minimise impact on life

Question 22

Pharmacological Treatment of Chronic Asthma

Escalation Pathway

Answer 22

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)

Question 23

Alternative Pharmacological Treatments for Asthma

Non-escalation pathway

Answer 23

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

Question 24

Prognosis of Asthma

Answer 24

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

Question 25

Definition of COPD

Answer 25

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

Question 26

Aetiology of COPD

Answer 26

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

Question 27

Chronic Bronchitis Pathophysiology

Answer 27

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

Question 28

Emphysema Pathophysiology

Answer 28

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

Question 29

Varieties of Emphysema

Answer 29

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

Question 30

Alpha-1 antitrypsin deficiency

Answer 30

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

Question 31

Pink Puffer

Answer 31

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

Question 32

Blue Bloater

Answer 32

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

Question 33

Presentation of COPD

Answer 33

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

Question 34

Respiratory Failure

Answer 34

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

Question 35

Cor Pulmonale or Pulmonary Hypertension

Answer 35

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

Question 36

Spirometry in COPD

Answer 36

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

Question 37

CXR in COPD

Answer 37

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’

Question 38

ABG in COPD

Answer 38

Often normal at rest

However upon exercise hypoxia +/- hypercapnia may be present

Question 39

General Treatment of COPD

Answer 39

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)

Question 40

Pharmacological Escalation Pathway for COPD

Answer 40

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

Question 41

Other Pharmacological Considerations in COPD

Answer 41

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

Question 42

Nocturnal Hypoxaemia

Answer 42

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

Question 43

Surgical Treatment of COPD

Answer 43

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

Question 44

Acute Exacerbation of COPD

Answer 44

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

Question 45

Asthma Vs. COPD

Answer 45

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