Respiratory 1 & 2 Flashcards
Complete control of asthma is defined as: (7)
- No day time symptoms
- No waking up at night due to asthma
- No asthma attacks
- Not needing rescue medication
- No limitation on activity/exercise
- PEFR >80% predicted
- Minimal side effects from medication
What structures comprise the large airways?
Trachea and primary bronchi
In what structures is the mucociliary escalator found?
The conducting zone - trachea, bronchi, and bronchioles
Within the conducting zone of the respiratory system, name one mechanism that aids purification of inhaled air and describe how it works
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.
The two main types of inhaler devices and how they work
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
MOA of Beta-2-Agonists (SABA/LABA)
Binds to beta 2 receptors in airway smooth muscle,mimicking adrenaline/noradrenaline to relax the smooth muscle of the bronchioles.
Example of a SABA and LABA
SABA = Salbutamol LABA = Salmeterol
Example of a SAMA and LAMA
SAMA = Ipratropium LAMA = Tiotropium
MOA of Muscarinic Antagonist
Blocks acetylcholine from binding to muscarinic (M3) receptors on smooth muscle, preventing bronchoconstriction and mucus secretion. (Blocks parasympathetic NS)
MOA of Corticosteroids
Mimic natural steroids in the body, up-regulate anti-inflammatory proteins and down-regulate pro-inflammatory proteins.
MOA of Leukotriene Receptor Antagonists (LTRAs)
Block leukotriene receptors, blocking the effects of leukotrienes in the airway.
4 main symptoms of asthma
- Wheeze
- Cough
- SOB
- Chest tightness/pain
When examining a patient with asthma, if they were presenting with an asthma attack, what may be heard on percussion and auscultation?
Percussion: Hyper-resonant lungs
Auscultation: High pitched, prolonged expiratorywheeze (gets louder with severity)
Except for Asthma, what other conditions may present with a wheeze?
Cystic Fibrosis, Heart Failure, Bronchial malignancy, COPD, Aspiration
Name ‘some’ triggers of asthma
Pets, Dust, Smoke, Cold Air, Exercise, GORD, Respiratory Tract Infections, Aspirin/NSAID hypersensitivity, Beta-blockers
Briefly describe the mechanism of the airway inflammatory response in asthma
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.
The 3 ways in which Leukotrienes play a key role in asthma.
- Inflammation
- Bronchoconstriction
- Mucus production
The 3 Leukotrienes that have been shown to be the most potentbronchoconstrictors
LTC4 ,LTD 4 and LTE 4
In asthma, what happens to the air way smooth muscle?
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.
Name the structures of the bronchi
Primary bronchi, Secondary bronchi, Tertiary bronchi, bronchiole/Terminal bronchiole
Which zone of the respiratory system is involved in gas exchange and what structures is it composed of?
Respiratory zone: Respiratory bronchiole, Alveolar Duct, Alveoli
Which zone of the respiratory system is NOT involved in gas exchange and what structures is it composed of?
The conducting zone - trachea, bronchi, and bronchioles
What features of asthma symptoms are you looking for when taking a history?
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
When considering asthma diagnosis what is the first line pulmonary function test?
Spirometry
What does an FeNO test measure?
Measures exhaled nitrous oxide, which is a marker of eosinophilic inflammation
When suspecting asthma, what does a direct bronchial challenge test involve?
Inhaling histamine/methacholine and then repeating spirometry to measure effect
The cell alveolar cell types and their functions
Type 1 = Aid in diffusion (95%)
Type 2 = Secrete surfactant, lowering surface tension and making it easier for alveoli to part and inflate (5%)
What is the respiratory membrane?
The site where gas exchange occurs - fused basement membranes of the alveoli epithelium and capillary endothelium
How does alveolar respiration maintain oxygen and carbon dioxide balance?
Large surface area with extremely thin walls, with a concentration gradient between oxygen and carbon dioxide
Define Type I Respiratory Failure
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
Define Type II Respiratory Failure
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
Describe the pathological changes in COPD
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.
Briefly describe the inflammatory cascade in COPD.
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.
What is Alpha 1 Antitrypsin Deficiency and what condition is it a risk factor for?
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!
Describe lung function changes in COPD/an obstructive lung disease
Dramatic reduction in FEV1
Reduced FVC
(but to a lesser extent than FEV1)
FEV1/FVC Ratio <0.7
Mechanisms of Bronchiectasis
Distinct phases of infection and chronic inflammation; causing excess mucus production and destruction of elastin, resulting in permanent dilatation and thickening of the airways.
Stepwise approach for treating COPD beyond SABA or SAMA if the patient has asthmatic features or evidence of steroid responsiveness….
Step 2 = ICS + LAMA
Step 3 = ICS, LABA + LAMA
Step 4 = Refer to specialist
SABA/SAMA kept for PRN throughout steps.
Stepwise approach for treating COPD beyond SABA or SAMA if the patient DOES NOT have asthmatic features or evidence of steroid responsiveness….
Step 2 = LABA and LAMA
Step 3 = ICS, LABA + LAMA
Step 4 = Refer to specialist
SABA/SAMA kept for PRN throughout steps.
MOA of carbocisteine and in what circumstances should it be considered?
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.
