Elm 16/17 Asthma Flashcards
Q: What is COPD?
A: COPD stands for Chronic Obstructive Pulmonary Disease. It involves the chronic narrowing of the airways, making it difficult to breathe.
Q: What are the main characteristics of COPD?
A: COPD is predominantly inflammatory and typically involves a combination of chronic bronchitis and emphysema. It is poorly reversible.
Q: What are some statistics related to COPD in the UK?
A: In the UK, COPD affects around 1.2 million people. The prevalence is growing, and a large number of cases may be undiagnosed. In 2012, nearly 30,000 deaths in the UK were attributed to COPD, with 86% of these deaths linked to smoking.
Q: What is chronic bronchitis?
A: Chronic bronchitis is characterized by a persistent cough with mucus production.
Q: What is emphysema?
A: Emphysema involves the destruction of tissues around the alveoli, the air sacs in the lungs where oxygen exchange occurs.
Q: What is bronchial asthma?
A: Bronchial asthma is a chronic condition characterized by the narrowing of the airways, which can occur in attacks or episodes.
Q: How is lung function measured in asthma?
A: Lung function in asthma is measured using tests such as FEV1 (forced expiratory volume in 1 second) and PEFR (peak expiratory flow rate). These tests involve taking a maximal breath in and blowing out as hard as possible.
Q: What are some statistics related to asthma in the UK?
A: In the UK, asthma affects around 5.4 million people, with approximately 200,000 having severe asthma. The annual NHS costs related to asthma exceed £1 billion. In 2017, nearly 1,500 deaths were attributed to asthma.
Q: What are some common triggers for asthma attacks?
A: Common triggers for asthma attacks include house dust mites, pollens, exercise, emotions, cold air, respiratory tract infections, animal fur, fungal spores, occupational factors, drugs, and pollutants.
Q: How is asthma categorized?
A: Asthma is divided into two categories: intrinsic (non-atopic/non-allergic) asthma and extrinsic (atopic/allergic) asthma.
Q: What structures support the trachea and bronchi?
A: The trachea and bronchi are supported by rings of cartilage. As you move down to the second and third bronchi, the cartilage turns into plates. Cartilage is absent at the bronchioles.
Q: What are the characteristics of bronchioles?
A: Bronchioles terminate at the alveoli and have much more smooth muscle, which plays a role in determining the diameter of the bronchioles.
Q: Describe the structure of a healthy airway.
A: A healthy airway includes a submucosal layer containing glands, smooth muscle, and an epithelial layer with goblet cells and ciliated epithelium. Cilia beat in a coordinated fashion to move dirt and mucus out of the lungs, although they are absent from the alveoli.
Q: How do asthmatic airways differ from healthy airways?
A: Asthmatic airways typically have more glands and muscles, with the submucosa infiltrated by immune system cells. Other characteristics include edema, a thicker basement membrane, loss of epithelium (resulting in fewer cilia and more goblet cells), and the formation of mucus plugs.
Q: What is plastic bronchitis?
A: Plastic bronchitis is a symptom present in many conditions characterized by the formation of mucus plugs in the airways.
Q: How does exercise relate to asthma attacks?
A: It’s argued that during exercise, large volumes of air are brought into the lungs via the mouth, bypassing the warming and humidifying effects of the nasal cavity. This can lead to dehydration of the airway surfaces, potentially triggering an asthma attack.
Q: Describe the process of allergic airway sensitization.
A: Allergic airway sensitization involves inhalation of an allergen, dendritic cells sampling the allergen and presenting pieces of it on their surface via MHCII, migration of dendritic cells to lymph nodes where they activate allergen-specific T cells, leading to clonal expansion and TH2 polarization. TH2 cells produce inflammatory cytokines that drive allergic inflammation and asthmatic responses.
Q: What are the characteristics of asthma attacks?
A: Asthma attacks are biphasic. The early phase involves bronchoconstriction, which can last up to 1.5 hours and is characterized by mast cell degranulation and increased acetylcholine from the parasympathetic nervous system. The later phase also involves bronchoconstriction and inflammation, which can be delayed up to 6 hours and includes the recruitment of leukocytes and production of inflammatory mediators.
Q: What do mast cells contain, and how are they activated?
A: Mast cells contain granules containing pre-formed mediators, along with other mediators from membrane lipids such as leukotrienes. Mast cells recognize antigens through IgE antibodies attached to their surface. When activated, antigen cross-links IgE, leading to degranulation.
Q: What immune cells are important in the later phase of asthma attacks, and what do they produce?
A: In the later phase of asthma attacks, eosinophils are important. They produce major basic protein and signaling molecules, which can lead to tissue damage, increased mucus production, airway remodeling, and sensitization.
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Q: What are some effects of mediators released during asthma attacks?
Ach and leukotrienes?
Chemotactic factors?
Major basic proteins?
A: During the early phase of asthma attacks, mediators such as acetylcholine and leukotrienes (C, D, and E4) cause contraction of airway smooth muscle, increased vascular permeability, and bronchial secretions. Chemotactic factors lead to the infiltration of lung tissue by neutrophils and eosinophils. In the later phase, these effects are amplified, along with epithelial desquamation and cell death caused by major basic protein from eosinophils.
Q: What is the stepped approach according to NICE guidelines for adult asthma management?
The stepped approach for adult asthma management according to NICE guidelines includes several steps:
For those experiencing less than three asthma attacks a week, a short-acting beta-agonist (SABA) is given.
If asthma remains uncontrolled with SABA alone, an inhaled corticosteroid (ICS) is added.
If asthma is still uncontrolled, a leukotriene receptor antagonist (LTRA) is added.
A long-acting beta-agonist (LABA) may be added if needed.
Maintenance and reliever therapy (MART) can be offered.
If asthma remains uncontrolled, the steroid dose may be increased.
High-dose ICS may be prescribed.
Additional treatments may be added.
If asthma is still not controlled, specialist advice should be sought.
Q: How are beta adrenoceptor agonists categorized mechanistically?
A: Beta adrenoceptor agonists are categorized mechanistically into bronchodilators (such as long-acting β2 agonists, theophylline, mAChR antagonists, and leukotriene antagonists) and anti-inflammatory drugs (including glucocorticosteroids and monoclonal antibodies).
Q: How are beta adrenoceptor agonists categorized into relievers and preventers?
A: Beta adrenoceptor agonists are categorized into relievers and preventers. Relievers, used for immediate relief, are typically short-acting beta agonists. Preventers, used for long-term management, mostly consist of glucocorticoids but may also include oral theophylline, leukotriene antagonists, and long-acting beta agonists alongside steroids.
Q: What efforts have been made to develop selective beta adrenoceptor agonists?
A: Efforts have been made to develop beta adrenoceptor agonists that are selective for either B1 or B2 receptors. It’s easier to develop agonists selective for B2 receptors, as modifying the structure of adrenaline, such as increasing the size of substituents or altering OH groups, can increase selectivity and reduce inactivation.
Q: What are some effects mediated by beta-adrenoceptors?
A: Effects mediated by beta-adrenoceptors include bronchodilation, cardiac stimulation, and metabolic effects such as glycogenolysis and lipolysis.
Q: What modifications have been made to adrenaline to develop selective B2 agonists?
A: Modifications to adrenaline to develop selective B2 agonists include increasing the size of substituents, replacing one of the OH groups with CH2OH, or changing its ring position. These modifications help reduce inactivation and increase selectivity for B2 receptors.
Q: What are SABAs and their characteristics?
A: SABAs, or short-acting beta-agonists, are bronchodilators with a duration of action of 4-6 hours. Examples include salbutamol and terbutaline. Salbutamol is 20-fold selective for B1 receptors. They are mainly delivered via metered dose inhaler (MDI).
Q: What are the uses of short-acting beta-agonists (SABAs)?
A: SABAs are used as reliever inhalers for immediate relief in asthma. They can be used as the sole drug if asthma symptoms occur twice a week or less, or they can be used in addition to preventers if symptoms are more frequent.
Q: What are LABAs and their characteristics?
A: LABAs, or long-acting beta-agonists, have a duration of action of 12 hours and are taken twice a day to prevent symptoms. NICE recommends that they are only given with glucocorticoids. Examples include salmeterol and formoterol, which is fast onset and long-acting and used in MART (maintenance and reliever therapy).
Q: What is the mechanism of salmeterol?
A: Salmeterol’s mechanism involves the terminal portion (exosite) of the alkylamine chain anchoring the molecule to the receptor, while the other end (active center) repetitively activates the receptor. Its lipophilicity (3200) allows it to dissolve into membranes and slowly leak out, remaining in tissues longer.
