Asthma and COPD Flashcards
When does an FEV1:FVC reading suggest airway resistance?
When it is less than 70-80%
What is PEF?
. Peak Expiratory Flow
. A person’s maximum speed of expiration
What is FEV1:FVC?
The proportion of a person’s vital capacity that they are able to expire in the first second of forced expiration
What is COPD a combination of?
Chronic bronchitis and emphysema (also associated with bronchopneumonia)
What is chronic bronchitis? How does it affect FEV1:FVC?
. Increased mucus, airway obstruction, intercurrent infections
. FEV1 reduced
What is emphysema?
Destruction of alveoli
Describe how a stimulus can lead to the early and late phases of an asthma attack.
. Stimulus triggers release of mast cells and mononuclear cells
. Activate spasmogens and chemotaxins
. Spasmogens release histamine, prostaglandins, leukotrienes, which cause bronchospasm (early phase)
. Chemotaxins release leukotrienes, which attract leukocytes (especially eosinophils), which leads to inflammation (late phase)
Describe how the early phase of an asthma attack is activated.
. Stimulus activates mast cells and mononuclear cells
. These activate spasmogens, which release histamine, prostaglandin D2, and leukotrienes C4 + D4
. Leads to bronchoconstriction and bronchospasm
Describe how the late phase of an asthma attack is activated.
. Stimulus activates mast cells and mononuclear cells
. These activate chemotaxins, which release leukotrienes (B4). These leukotrienes attract leuokocytes, especially eosinophils, and mononuclear cells, which leads to inflammation and airway hyperactivity
What are prostaglandin D2 and leukotrienes C4 and D4?
Bronchoconstrictors
What do bronchodilators do? When can they be taken?
. Reverse bronchospasm (early phase)
. Rapid relief
. Take when having asthma attack or prior to an event known to cause an attach
What do preventors do? When can they be used?
. Prevent asthma attack, can be anti-inflammatory
. Can’t be used during an attack
Describe the mechanism of action of salbutamol.
. Binds to B2-adrenoceptor on bronchial smooth muscle
. Causes increase in cAMP (second messenger), which causes bronchial smooth muscle to relax
How is bronchial smooth muscle relaxation stopped?
. PDE (phosphodiesterase) breaks down cAMP to AMP
. This stops bronchial relaxation
How is down-regulation of B2-agonists controlled?
Patients given steroid to take as well as B2-agonist
What is the difference between salbutamol and salmeterol?
Salbutamol is a short-term treatment for asthma, salmeterol is a LABA used for long term treatment
Can you give salbutamol long-term?
No, as this leads to increased mortality. If long-term treatment needed, should use LABAs such as salmeterol
What is first line treatment for asthma?
B2-agonists, salbutamol or salmeterol
What is second choice treatment for asthma?
. Xanthines e.g. theophylline
. These are bronchodilators, not as good as B2-agonists
What other choices are there for asthma treatment after first and second line options?
Muscarinic M-receptorantagonists, corticosteroids, LTRAs (leukotriene receptor antagonists), omalizumab
How do muscarinic M-receptor antagonists work? What are the usually used for?
. Block parasympathetic bronchoconstriction (normally ACh would bind to M3-receptors on bronchial smooth muscle to activate bronchoconstriction)
. Usually used for COPD, not asthma
What are LTRAs?
Leukotriene receptor antagonists, prevent leukotrienes from causing bronchospasm and inflammation
Can asthmatics take NSAIDs? Why is this?
No because NSAIDs increase leukotriene production, which can provoke asthma
Give two examples of NSAIDs.
Aspirin and Ibuprofen
