Respiratory 1 & 2

Question 1

Complete control of asthma is defined as: (7)

Answer 1

1. No day time symptoms
2. No waking up at night due to asthma
3. No asthma attacks
4. Not needing rescue medication
5. No limitation on activity/exercise
6. PEFR >80% predicted
7. Minimal side effects from medication

Question 2

What structures comprise the large airways?

Answer 2

Trachea and primary bronchi

Question 3

In what structures is the mucociliary escalator found?

Answer 3

The conducting zone - trachea, bronchi, and bronchioles

Question 4

Within the conducting zone of the respiratory system, name one mechanism that aids purification of inhaled air and describe how it works

Answer 4

The mucociliary escalator - composed of mucous-producing goblet cells and ciliated epithelium which work in conjunction to trap and remove inhaled particles including pathogens before they can reach the lung tissue.

Question 5

The two main types of inhaler devices and how they work

Answer 5

Metered dose inhaler (pMDI):Drug is contained in an propellant which shoots it into the lungs.

Dry powder inhaler: Deliver medicine as a dry powder; patient breathing inaerosolises the drug so it can get into the lungs

Question 6

MOA of Beta-2-Agonists (SABA/LABA)

Answer 6

Binds to beta 2 receptors in airway smooth muscle,mimicking adrenaline/noradrenaline to relax the smooth muscle of the bronchioles.

Question 7

Example of a SABA and LABA

Answer 7

SABA = Salbutamol
LABA = Salmeterol

Question 8

Example of a SAMA and LAMA

Answer 8

SAMA = Ipratropium
LAMA = Tiotropium

Question 9

MOA of Muscarinic Antagonist

Answer 9

Blocks acetylcholine from binding to muscarinic (M3) receptors on smooth muscle, preventing bronchoconstriction and mucus secretion. (Blocks parasympathetic NS)

Question 10

MOA of Corticosteroids

Answer 10

Mimic natural steroids in the body, up-regulate anti-inflammatory proteins and down-regulate pro-inflammatory proteins.

Question 11

MOA of Leukotriene Receptor Antagonists (LTRAs)

Answer 11

Block leukotriene receptors, blocking the effects of leukotrienes in the airway.

Question 12

4 main symptoms of asthma

Answer 12

1. Wheeze
2. Cough
3. SOB
4. Chest tightness/pain

Question 13

When examining a patient with asthma, if they were presenting with an asthma attack, what may be heard on percussion and auscultation?

Answer 13

Percussion: Hyper-resonant lungs

Auscultation: High pitched, prolonged expiratorywheeze (gets louder with severity)

Question 14

Except for Asthma, what other conditions may present with a wheeze?

Answer 14

Cystic Fibrosis, Heart Failure, Bronchial malignancy, COPD, Aspiration

Question 15

Name ‘some’ triggers of asthma

Answer 15

Pets, Dust, Smoke, Cold Air, Exercise, GORD, Respiratory Tract Infections, Aspirin/NSAID hypersensitivity, Beta-blockers

Question 16

Briefly describe the mechanism of the airway inflammatory response in asthma

Answer 16

Allergen detected by dendritic cell, which is an antigen presenting cell.

Dendritic cell phagocytoses allergen and presents it via MHC II complex to T-lymphocyte.

Various cytokines (interleukins) released which recruits basophils, mast cells and eosinophils.

Mast cell degranulate and release histamine and leukotrienes (inflammatory mediators which cause - Inflammation, Bronchoconstriction
and Mucus production) which recruit more immune cells.

Eosinophils also release leukotrienes AND proteases which causes damage over time in chronic asthma.

Question 17

The 3 ways in which Leukotrienes play a key role in asthma.

Answer 17

1. Inflammation
2. Bronchoconstriction
3. Mucus production

Question 18

The 3 Leukotrienes that have been shown to be the most potentbronchoconstrictors

Answer 18

LTC4 ,LTD 4 and LTE 4

Question 19

In asthma, what happens to the air way smooth muscle?

Answer 19

Increase in airway smooth musclecell size and number as well as enhanced proliferation and migration.

Presence of inflammatory mediators and thus inflammation causes the airway smooth muscle to become hyper-responsive.

Question 20

Name the structures of the bronchi

Answer 20

Primary bronchi, Secondary bronchi, Tertiary bronchi, bronchiole/Terminal bronchiole

Question 21

Which zone of the respiratory system is involved in gas exchange and what structures is it composed of?

Answer 21

Respiratory zone: Respiratory bronchiole, Alveolar Duct, Alveoli

Question 22

Which zone of the respiratory system is NOT involved in gas exchange and what structures is it composed of?

Answer 22

The conducting zone - trachea, bronchi, and bronchioles

Question 23

What features of asthma symptoms are you looking for when taking a history?

Answer 23

Symptoms are worse at night and in the early morning;
Symptoms are present in response to exercise, allergen exposure and cold air;
Symptoms are present after taking NSAIDs/aspirin or beta-blockers.
History of atopic disorder (Eczema, hay fever)
Family history of asthma/atopic disorder

Question 24

When considering asthma diagnosis what is the first line pulmonary function test?

Answer 24

Spirometry

Question 25

What does an FeNO test measure?

Answer 25

Measures exhaled nitrous oxide, which is a marker of eosinophilic inflammation

Question 26

When suspecting asthma, what does a direct bronchial challenge test involve?

Answer 26

Inhaling histamine/methacholine and then repeating spirometry to measure effect

Question 27

The cell alveolar cell types and their functions

Answer 27

Type 1 = Aid in diffusion (95%)

Type 2 = Secrete surfactant, lowering surface tension and making it easier for alveoli to part and inflate (5%)

Question 28

What is the respiratory membrane?

Answer 28

The site where gas exchange occurs - fused basement membranes of the alveoli epithelium and capillary endothelium

Question 29

How does alveolar respiration maintain oxygen and carbon dioxide balance?

Answer 29

Large surface area with extremely thin walls, with a concentration gradient between oxygen and carbon dioxide

Question 30

Define Type I Respiratory Failure

Answer 30

Type I = Hypoxemia, with normal or low Co2.

Pco2 <60 mmHg, despite giving 60% O2.

Oxygen is able to get into the alveoli, but is unable to get into the bloodstream very well, hence hypoxemia.

Causes: V/Q Mismatch, Shunting, Diffusion Limitation, Alveolar Hyperventilation

Question 31

Define Type II Respiratory Failure

Answer 31

Type II = Alveolar ventilation is insufficient to excrete the carbon dioxide being produced. (obstruction, decreased respiratory drive), so Co2 will collect, hence hypercapnia. PaCO2 > 50mmHg

Question 32

Describe the pathological changes in COPD

Answer 32

Chronic Bronchitis = Excessive mucus production and inflammation of the lining of the bronchial tubes.

Emphysema = Alveolar destruction, resulting in enlargement of airspace and reduction in gas exchange area.

Question 33

Briefly describe the inflammatory cascade in COPD.

Answer 33

The precipitating event causes inflammation of the airway epithelium

Activation of the resident immune cells including macrophages and T cells.

Recruitment of resident immune cells that release cytotoxic granular contents, reactive oxygen species and proteinases; contributing to mucus secretion and small airway remodelling.

Question 34

What is Alpha 1 Antitrypsin Deficiency and what condition is it a risk factor for?

Answer 34

Genetic disorder which causes the Alpha 1 Antitrypsin protein to be defective or absent.

Alpha 1 Antitrypsin normally functions as a protease inhibitor which functions to inativase elastase in response to lung inflammation.

Deficiency means that neutrophil elastase isn’t inactivated, which leads to elastin break down – this primarily affects the alveoli, causing airspace enlargement.

Genetic risk factor for Emphysema!

Question 35

Describe lung function changes in COPD/an obstructive lung disease

Answer 35

Dramatic reduction in FEV1

Reduced FVC
(but to a lesser extent than FEV1)

FEV1/FVC Ratio <0.7

Question 36

Mechanisms of Bronchiectasis

Answer 36

Distinct phases of infection and chronic inflammation; causing excess mucus production and destruction of elastin, resulting in permanent dilatation and thickening of the airways.

Question 37

Stepwise approach for treating COPD beyond SABA or SAMA if the patient has asthmatic features or evidence of steroid responsiveness….

Answer 37

Step 2 = ICS + LAMA

Step 3 = ICS, LABA + LAMA

Step 4 = Refer to specialist

SABA/SAMA kept for PRN throughout steps.

Question 38

Stepwise approach for treating COPD beyond SABA or SAMA if the patient DOES NOT have asthmatic features or evidence of steroid responsiveness….

Answer 38

Step 2 = LABA and LAMA

Step 3 = ICS, LABA + LAMA

Step 4 = Refer to specialist

SABA/SAMA kept for PRN throughout steps.

Question 39

MOA of carbocisteine and in what circumstances should it be considered?

Answer 39

Break down mucus by making it thinner and irritate the mucosa to stimulate clearance, i.e. coughing up. Contraindicated in peptic ulceration (due to irritating mucosa)

Should be considered in a COPD patient with chronic sputum production.