Unit 13 Week 1 Flashcards
What is asthma
- characterized by paroxysmal (fits of) and reversible obstruction of the airways
- now increasingly understood as an inflammatory condition
- combined with bronchial hyperresponsiveness such as bronchospasm and excessive production of secretions
“Chronic eosinophilic bronchitis”
What are the types of asthma (8)
Allergic or atopic
Seasonal
Occupational
Non-allergic
Exercise induced
“difficult asthma”
Asthma COPD overlap
Cough variant
allergic or atopic asthma
triggered by allergens such as pollen, pets and dust, most commonly these patients will also suffer from hay fever, eczema and food allergies alongside this
Atopy = the genetic tendency to develop allergic disease
Eosinophillic – typically high levels of eosinophils and IgE in the blood
Doesn’t always involve eosinophils – neutrophilic and basophilic asthma
Seasonal asthma
flare ups during certain times of the year such as during hay fever season or when it is cold
Occupational asthma
usually first diagnosed as an adult and symptoms improve the days that they are not at work
non allergic asthma
often develops later in life and can be more severe, but causes are not well understood
“difficult asthma”
symptoms do not go away even with high doses of medication, frequent asthma attacks
Asthma can also be categorised by its onset (2)
Adult
Childhood
What is the staging system for asthma
Mild intermittent asthma – mild symptoms of asthma occur no more than two days per week to two times per month
- Mild persistent asthma – mild symptoms occur more often than twice per week
- Moderate persistent asthma – increasingly severe symptoms of asthma occur daily and at least one night each week – flare ups also last several days
- Severe persistent asthma – symptoms occur several times per day almost every day
Allergenic triggers for asthma
mediated by IgE responses leading to mediator release causing inflammation, capillary leakage into the airways, increase in mucus secretion and bronchial smooth muscle contraction
- Dust mite faeces
- pollen
- pet fur
- Food stuffs
- etc.
Non-allergenic triggers for asthma
mediated by bronchospasm due to increased parasympathetic vagal tone
- Cold/ dlu symptoms
- cigarette smoke
- air pollution
- meteorologiocal changes- changes in temperature
- occupation exposures- e.g., working in a bakery or carpenters
- drugs- analgesics, NSAID’s
- Stress and emotional disturbance
- exercise
- time of day- natural dip in peak flow overnight may lead to nocturnal waking
Symptoms of asthma
Variable with time and intensity
Wheezing
shortness of breath
chest tightness
cough
diurnal episodes (waking up at night due to worsening)
between exacerbations most patients are asymptomatic
Pathophysiology of asthma 1st exposure
Type 1 hypersensitivity
Harmless primary exposure
- Allergen is phagocytosed by an antigen presenting cell (e.g., a dendritic cell at a mucosal surface) and presented on MHC II.
- Presented to naive T cells causing them to become Th2
a) T cells release cytokines (Il-4) which cause B cells to class switch to produce IgE
b) They also release Il-5 which stimulates locally recuited eosinophils
c) IL-13 – stimulates mucous secretion from bronchial submucosal glands and promote IgE production from B cells.
- T cells and epithelial cells secrete chemokines that recruit more T cells and eosinophils – this exacerbates the reaction
- IgE specific to that antigen binds to Fc receptors of submucosal mast cells.
- Allergen is cleared from the body mainly by IgE
Pathophysiology of asthma 2nd exposure
- Antigen binds to the variable region on IgE molecules on mast cells surfaces
- Cross-linking of multiple IgE molecules which enhances signalling into mast cell.
- Mast cell releases its granule contents which have immediate effect.
- Mast cells also synthesise other inflammatory mediators
Early phase hypersensitivity reaction
Dominated by:
by bronchoconstriction – triggered by direct subepithelial vagal receptors through both central and local reflexes triggered by mediators produced by mast cells and other cells in the reaction.
o increased mucus production
o variable degrees of vasodilation
o increased vascular permeability.
Late phase hypersensitivity
dominated by:
o Recruitment of leukocytes – eosinophils, neutrophils, and T cells
o Th17 cells recruit neutrophils.
Substances that cause bronchoconstriction
- Leukotrienes- C4, D4, E4 (also increase mucous secretions and vascular permeabilty)
- Acetylcholine- released from transpulmonary parasympathetic neurones by stimulating smooth muscarinic receptors
- Histamine
- Porstaglandin- also vasodilates
- Platelet activating factor- aggregation of platelets
As the inflammation goes on it causes airway dysfunction and through the release of chronic inflammatory mediators causes remodeling of the airway wall. Name some of those changes:
Mucous gland enlargement
Smooth muscle hyperplasia
Angiogenesis
Fibrosis
What should a healthy spirometry (flow volume loop) look like
- Volume as Y axis
- Flow as X axis
- Roughly an oval rhough +ve and -ve axis, higher than wide
- Expiration on top
- Inspiration on bottom
What does an obstructive flow volume loop look like
Pre bronchodilator:
