Nature Of Airway Obstructon

Question 1

How can airways become obstructed?

Answer 1

Hypertrophy of the muscle in the structure
Narrowing of the lumen of the airways due to mucus or foreign bodies
Destruction of surrounding or supporting structures

Question 2

How do the airways change from central to peripheral?

Question 3

What are the obstructive conditions of the airways?

Answer 3

Bronchieactasis
Emphysema
Asthma

Question 4

What is the most common obstructive airway disease?

Answer 4

Asthma

Question 5

What is asthma?

Answer 5

Exposure to allergen which is taken up by dendritic cells that presents to Th2 cells. Chronic inflammation of the airways characterised by a Th2 immune response that increases IL-4, IL-5, IL-13 which initiates eosinophil activation and mast cell degranulation for bronchoconstriction of the airways.

It causes wheeze, shortness of breath, chest tightness, and cough with limitation of expiratory flow.

Question 6

What are the acute changes in asthma?

Answer 6

Inflammatory mediators act on airway structures such as tissue and blood vessels for:
Vasodilation, plasma leakage and oedema
Mucus hypersecretion
Sensory nerve activation due to exposure to triggers results in reflex bronchoconstriction, by cholinergic receptors.

Question 7

What are the chronic changes in asthma?

Answer 7

Subepithelial fibrosis and smooth muscle hypertrophy.

Question 8

How is asthma diagnosed?

Answer 8

Performing reversibility testing. This is done by using spirometry for testing lung function before medication and after medication of a bronchodilator. If lung function improves, it indicates obstructive lung disease.

Question 9

What patient signs and symptoms are used for asthma diagnosis?

Answer 9

History of a wheeze and variable PEF or FEV1.
History of atopy
Recurrent episodes of symptoms with variability.
Absence of symptoms of alternative diagnosis

Question 10

How can peak expiratory flow rate be used?

Answer 10

Peak expiratory flow meter is used to measure flow rate of air in a forceful expiration which provides an indication of ventilation adequacy and airflow obstructive diseases only. PEFR is typically higher in male patients and taller patients.

The measures are effort dependent and vary depending on the meter used. It is important that patients report it twice daily for 2-4 weeks.

Question 11

How can the peak expiratory flow rate variability be measured?

Answer 11

Difference between Highest reading - lowest reading/ mean of the highest and lowest days.

Question 12

What is significant PEFR variability?

Answer 12

10-20% variability is the upper limit of normal PEFR range. Any greater is considered concerning.

Question 13

How is bronchoconstriction assessed in diagnostic testing?

Answer 13

Administration of mannitol via inhalation results in the release of inflammatory mediators such as histamine and prostaglandins. For those with hyperreactivity in asthma, this results in bronchoconstriciton.

Bronchoconstriction is a key feature in asthma triggered by an allergen or exertion such as exercise. This causes an increase in osmolarity and dehydration that mannitol mimics.

Question 14

How is eosinophilic inflammation assessed in diagnostic testing?

Answer 14

Fractional exhaled nitric oxide, a value for the level of inflammation in the lungs by the levels of the inflammatory mediator nitric oxide present in breath.

Question 15

What is mannitol?

Answer 15

An osmotic diuretic used to decrease intracranial pressure. It acts on the PCT and Loop of Henle to reduce water re-absorption, with a loss of Na+. Due to a loss of water, there are more solute particles per litre, which results in an increase of osmolarity.

Question 16

Which are the tests for atopy?

Answer 16

Blood test for total IgE levels and radioallergosorbent test
Skin prick test

Question 17

What are the types of asthma?

Answer 17

Atopic asthma
Non-allergic asthma
Persistent limitation asthma
Asthma and obesity

Atopic asthma is the most common type.

Question 18

What are the features of atopic asthma?

Answer 18

Identifiable triggers with childhood onset and driven by eosinophilic inflammation. It is the most common form of asthma

Question 19

What are the features of non-atopic asthma?

Answer 19

Less common form of asthma triggered by exertion or infection. There is an absence of an eosinophilic response and is driven by neutrophil influx

Question 20

What is persistent limitation asthma?

Answer 20

Asthma with persistent airflow obstruction is when treatment fails to reverse or only incompletely reverses airflow obstricton that has an unknown cause. This is a feature also present in COPD.

Question 21

What is the link between asthma and obesity?

Answer 21

Obesity results in systemic inflammation and mechanically results in airway narrowing and resistance, with little presence of eosinophilic inflammation.

Question 22

What is COPD?

Answer 22

Irreversible expiratory airflow obstruction in the lungs which limits expiration and results in hyper expansion of the lungs due to loss of elastic recoil and airway narrowing from inflammation. There is a severely reduced FEV1, with a low FEV that results in a FEV1/FVC ratio of less than 0.7.

Over time, the chronic hypoxia can lead to pulmonary hypertension.

Question 23

What is the presentation of COPD?

Answer 23

It is characterised by dyspnoea, chronic cough, that may be productive, recurrent wheeze, weight loss, fatigue and chest tightness.

Question 24

What are the risk factors for COPD?

Answer 24

Smoking
Abnormal lung development
Genetic predisposition

->These result in acute exacerbations of respiratory symptoms and COPD is linked to chronic comorbidities such as cor pulmonale, which is right sided heart failure due to hypoxaemia inducing vasoconstriction.

Question 25

What are the types of COPD?

Answer 25

Chronic bronchitis Emphysema

Question 26

What is the structure of the bronchi?

Answer 26

Consists of the Mucosa: pscaudostratified columnar epithelia with cilia and lamina propr.. Submucosa: smooth muscle connective tissue and mucinous, glands Cartilage in bronchi to keep it open

Question 27

What is the lamina propria?

Answer 27

Loose connective tissue and basement membrane in the mucosa.

Question 28

What is the pathophysiology of chronic bronchitis?

Answer 28

Exposure to irritants such as cigarette smoke results in the hypertrophy and hyperplasia of mucinous glands for mucus hypersecretion that causes narrowing of the lumen. Cilia are less mobile and this disrupts the mucociliary escalator, causing air trapping.

Question 29

What is the presentation of chronic bronchitis?

Answer 29

Early morning cough and excessive mucus production for 3 moths in 2 consecutive years Bronchospasm results in wheeze, crackles, hypoxaemia and hypercapnia. Patients may have features of cyanosis and obesity. Most patients have normal lung capacity, functional residual capacity and residual volume

Question 30

What are the findings for chronic bronchitis on examination?

Answer 30

tachypnoea with accessory muscle use Coarse crackles Barrel chest due to hyperinflation Asterixis where CO2 retention occurs

Question 31

What is a complication with chronic bronchitis?

Answer 31

hypoxaemia from a V/Q mismatch results in polycythaemia with hypoxia pulmonary vasoconstriciton that can lead to right sided heart failure and peripheral oedema.

Question 32

What is used to diagnose chronic bronchitis?

Answer 32

spirometry showing irreversible obstructive pattern, where FEV1: FVC ratio is less than 0.7 Pulse oximetry CXR showing flattened diaphragm and increased intercostal spacing FBC for ABG and haemotoogical

Question 33

What is the treatment of chronic COPD?

Answer 33

SABA SAMA: short acting muscarinic antagonist such as ipatropium Supplemental oxygen Antibiotics

Question 34

What is used to score the severity of COPD?

Answer 34

CAT score: Prescence of productive cough which impairs sleep, activity, confidence and energy

Question 35

What pharmacological agent is given for COPD exacerbations?

Answer 35

Roflumilast, a selective phosphodiesterase inhibitor In chronic bronchitis, mucolytics like carbocisteine and erdosteine

Question 36

What is the pathophysiology of emphysema?i

Answer 36

Progressive destruction of alveolar spectacular and capillaries, caused by exposure to irritants which increase production of inflammatory mediators such as leukotrine B4, IL-8 and TNF-alpha and recruitment of neutrophils that release protease. There is an imbalance between proteases and antiproteases that causes degradation of collagen and elastin with damage to alveoli and loss of septation. This diminishes gas exchange and alveoli damage means lungs are more compliant and hyperinflate. Air leaving the lungs at high velocity exerts pressure on alveoli that become prone to collapse.

Question 37

What is a consequence of emphysema?

Answer 37

development of enlarged airways and airspace’s known as bullae, with decreased lung elastic recoil and increased ris of collapse. The hyperinfaltin increases expiratory airflow and increased FRC and RV with barrel chest and purse-lipped breathing.

Question 38

Which part of the lung is affected in emphysema?

Answer 38

Acinus, which is the distal most part of the airway of the lungs responsible for gas exchange.

Question 39

What is the most common type of emphysema?

Answer 39

Centrilobular emphysema which affects the central/proximal acini of the central and upper lobe of the lungs, associated with cigarette smoking.

Question 40

What is panacinar emphysema?

Answer 40

Due to genetic a1-antitrypsin deficiency, affecting the entire acinus of the lower lung lobes.

Question 41

What is paraseptal emphysema?

Answer 41

Paraseptal emphysema occurs on the periphery of the lobules, with a risk of rupture and pneumothorax.

Question 42

What are the findings for emphysema?

Answer 42

distant breath sounds with expiratory wheeze Normal blood gas at rest, with oxygen desaturation during exertion Hyper inflated lungs with flat diaphragm and increased anterior-posterior diameter ribs (barrel chest)

Question 43

What is the management of emphysema?

Answer 43

bronchodilators with B2 agonists and anticholinergic Pulmonary rehabilitation O2 therapy Prevention of COPD exacerbations with pneumococcal and influenza vaccination Infections managed with short course of oral corticosteroids to improve lung function with antibiotcs

Question 44

What is bronchieactasis?

Answer 44

Widening of the bronchi that occurs due to an initial injury that results in inflammation, making it pre-disposed to repeated infection that drive mucuous hypertrophy and hypersecretion. The injured epithelia also impacts the cilia and impairs the mucociliary escalator. High neutrophil count drives this process because their recruitment releases proteases which cause further damage.

Question 45

What are the characteristics of Bronchieactasis?

Answer 45

Chronic purulent cough, with dyspnoae and wheezing and potential for haemoptysis.

Question 46

Which conditions pre-dispose to Bronchieactasis?

Answer 46

Cystic fibrosis due to a mutation of the CFTR- gene for chloride transport which results in an impaired mucociliary apparatus that makes the airways more prone to infection and damage. Primary ciliary dyskinesia Alpha-1 trypsin deficiency

Question 47

What is primary ciliary dyskinesia?

Answer 47

Inherited genetic disorder affecting the structure of the cilia, disrupting the mucociliary apparatus and this increases infection risk. There is a characteristic situs invertus, where the organs are flipped to the opposite side.

Question 48

What are the differences between asthma and COPD?s

Answer 48

Asthma is driven by chronic inflammation and a eosinophilic and CD4 mediated response that can lead to reversible airflow obstruction, wheezing and COPD is airflow obstruction mediated by macrophages, neutrophils and CD8 cells, which can typically be alleviated by smoking cessation. Corticosteroids are ineffective in COPD.

Question 49

What is the overlap between asthma and COPD?

Answer 49

Presentation of symptoms are similar, with wheezing, dyspnoea and productive cough. They can both be treated with bronchodilators and muscarinic antagonists.