WEEK 2: Nature of airways obstruction Flashcards
State the types of airway obstructions.
Large airway obstruction (0-16 generation)
Small airway obstruction (> 17 generation)
Describe the structure of airway generations from the trachea to the alveolar sacs (Generation 0-23)
0: Trachea
1: Main bronchi (right and left)
2: Lobar bronchi (secondary bronchi)
3: Segmental bronchi (tertiary bronchi)
4: Bronchioles
6-16: Terminal bronchioles
17-19: Respiratory bronchioles
20-22: Alveolar ducts
23: Alveolar sacs
Statethe 4 forces body has to work against for breathing to occur.
State the 3 main components involved in airflow limitation.
Body has to work against 4 forces for breathing in to occur.
-Elastic recoil of the lungs
-Inertia of the respiratory system
-Surfaces forces
-Resistance of airways
IN OBSTUCTIVE DISEASES THERE IS increased resistance to airway flow
CAUSED BY
*Luminal obstruction: Increased secretion, airway thickening and narrowing due to inflammation
*Airway wall: muscle contraction in asthma
*Supporting structures surrounding the airway:
Airway obstruction:
Define Bronchial hyper-responsiveness.
How do we assess it?
What is PD20?
A state characterized by easily triggered bronchospasms.
Use provocation test by inhaling gradual increasing concentration of methacholine or histamine.
HISTAMINE: Triggers bronchoconstriction and mucosal secretion by acting on the H1 receptors.
METHACHOLINE: Acts on the M3 receptors.
Dose of the agonist [provocation dose] necessary to produce 20% fall in FEV1 is called PD20.
The dose of the agonist required to produce a 20% fall in Forced Expiratory Volume in 1 second (FEV1) is referred to as the PD20.
Patients with bronchial asthma respond to very low doses of histamine.
What are Atopy disorders?
Production of IgE in response to an allergen.
Atopy refers to a genetic predisposition to develop allergic hypersensitivity reactions to common environmental allergens.
What is bronchial asthma?
Bronchial asthma, commonly referred to as asthma, is a chronic respiratory condition characterized by inflammation of the airways (bronchi and bronchioles) and increased responsiveness to various stimuli.
This heightened sensitivity results in episodes of bronchoconstriction (narrowing of the airways) and increased mucus production, leading to symptoms such as wheezing, shortness of breath, chest tightness, and coughing.
Discuss atopy disorders.
Outline causes of atopy
Group of disorders including asthma and hay fever:
*Run in families
*Wealing skin reactions to common allergens
*Circulating plasma antibodies that can be transferred to the skin of non-sensitized individuals
Occupational sensitization [workers in isocyanate, latex industries]
Non-specific factors
Cold air and exercise
Atmospheric pollution and irritants, dust, vapor, fumes
Diet
Emotion
Drugs e.g. NSAID
Beta blockers
Compare intrinsic vs extrinsic asthma.
- Intrinsic Asthma:
Triggers:
*Non-allergic Factors: Intrinsic asthma is often triggered by non-allergic factors such as respiratory infections, exercise, cold air, stress, irritants (tobacco smoke, air pollution), and exposure to certain medications (aspirin and nonsteroidal anti-inflammatory drugs).
Onset:
Adult Onset: Intrinsic asthma often develops in adulthood, and individuals with this type may not have a history of allergies or a family history of asthma.
Immunological Response:
Less Involvement of Allergic Mechanisms: Intrinsic asthma is characterized by a less prominent role of allergic mechanisms. The immune response in intrinsic asthma is often more related to non-specific triggers and irritants.
Symptoms:
Variable Symptoms: Symptoms of intrinsic asthma can be variable and may not always follow a predictable pattern. Exacerbations may occur in response to specific non-allergic triggers.
Extrinsic Asthma:
*Triggers:
Allergens: Extrinsic asthma, also known as allergic asthma, is primarily triggered by exposure to allergens such as pollen, dust mites, animal dander, mold spores, and certain foods. Allergic reactions play a significant role in the development of symptoms.
Onset:
Childhood Onset: Extrinsic asthma often begins in childhood, and individuals with this type may have a personal or family history of allergies, eczema, or allergic rhinitis.
Immunological Response:
Allergic Mechanisms: Allergic mechanisms, involving the production of immunoglobulin E (IgE) antibodies and the release of inflammatory mediators, play a crucial role in extrinsic asthma. The immune response is more specific to allergens.
It is a type I hypersensitivity.
Symptoms:
Consistent Allergic Triggers: Extrinsic asthma symptoms may be more consistently triggered by exposure to specific allergens, leading to a more predictable pattern of symptoms.
Outline clinical features of bronchial asthma.
Reversible, episodic bronchospasm
Bronchial hypersensitivity to stimuli
Persistent bronchial inflammation
Chronic inflammatory disease of airways
Episodic dyspnea, cough, wheeze
Describe the inflammatory events in bronchial asthma.
- Allergen Exposure:
Individuals with allergic asthma are initially exposed to specific allergens, such as pollen, dust mites, animal dander, or certain foods. - Immune Response and Sensitization:
The immune system recognizes the allergen as foreign, leading to the activation of T-helper 2 (Th2) cells.
Th2 cells release cytokines, including interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13). - IgE Production and Mast Cell Sensitization:
*IL-4 stimulates B cells to produce immunoglobulin E (IgE) antibodies.
*IgE antibodies attach to mast cells, particularly on the surface of respiratory mucosa.
IgE also stimulates eosinophil release.
- Re-exposure to Allergen:
Upon re-exposure to the same allergen, the allergen binds to IgE antibodies on the surface of sensitized mast cells.
Early Phase Response (30-60 minutes):
*Mast Cell Degranulation: Cross-linking of IgE on mast cells triggers mast cell degranulation.
*Release of Primary and secondary Mediators: Primary mediators, including histamine, are rapidly released.
*Parasympathetic Bronchoconstriction: Histamine, along with other mediators, leads to the contraction of smooth muscles in the bronchioles, causing bronchospasm.
*Vasodilation and Increased Permeability: Histamine also causes vasodilation and increased permeability of blood vessels, contributing to edema and mucus production.
Late Phase Response (4-8 hours):
Secondary Mediators: Secondary mediators, such as leukotrienes and prostaglandins, are released later in the inflammatory response.
State the early phase mediators and their functions.
- Leukotrienes (C4, D4, E4):
Bronchoconstriction: Contribute to the contraction of smooth muscles in the bronchioles.
Increased Vascular Permeability: Enhance the permeability of blood vessels, leading to edema.
Increase Mucin Production: Stimulate the production of mucus, contributing to airway obstruction.
- Prostaglandins (D2, E2, F2):
Bronchoconstriction: Contribute to smooth muscle contraction in the airways.
Vasodilation: Cause dilation of blood vessels.
Histamine Release: May enhance the release of histamine.
- Histamine:
Bronchospasm: Contributes to the contraction of smooth muscles in the bronchioles.
Increased Permeability: Leads to increased permeability of blood vessels, contributing to edema.
State the late phase mediators and their function in asthma.
- Leukotriene B4:
*Chemotactic Agent: Attracts immune cells, particularly eosinophils, to the site of inflammation.
- Interleukin-4 (IL-4) and Interleukin-5 (IL-5):
*Enhance IgE Production: IL-4 and IL-5 play roles in promoting the production of IgE antibodies.
- Tumor Necrosis Factor-alpha (TNF-α):
*Pro-inflammatory: Contributes to the recruitment and activation of immune cells, as well as the amplification of the inflammatory response.
Discuss airway obstruction in asthma.
*Bronchospasm
*Mucosal oedema
*Retained secretion
Discuss Bronchial asthma diagnostic symptoms.
*Asthmatic attack
*Status asthmaticus
ASTHMATIC ATTACK
Wheeze, dyspnea, dry cough, tachycardia.
Prolonged expiration
Use of accessory muscles
Hyperinflated chest
STATUS ASTHMATICUS
Severe attack: exhaustion and fear, inability to speak, drowsiness, cyanosis, tachycardia, reduced breath sounds, “silent” chest.
What is status asthmaticus?
Status Asthmaticus is a severe form of asthma characterized by an asthma attack that doesn’t improve with traditional treatments, such as inhaled bronchodilators.
