Session 6- Obstructive Lung Diseases Flashcards
(26 cards)
what is asthma
a chronic inflammatory disorder of the airways characterised by intermittent airway obstruction.
Obstruction of the airways- reversible
what is the difference between the obstruction inn COPD and asthma
in asthma its reversible- improves with bronchodilators
Pathophysiology of asthma
Macrophages process and present antigens to t lymphocytes
This activates T cells with Th2 cells being preferentially activated
Th2 cells release cytokines which attract and activate inflammatory cells
Th2 cells activate B cells which produce IgE
Exposure to antigen results in a 2 phase response consisting of an intermediate response followed by a late phase response
What inflammatory cells are involved in asthma
Th2 cells aka Cd4+
What is The immediate response and what causes it
Type 1 hypersensitivity
Caused by an interaction of the allergen and specific IgE antibodies leading to mast cells degranulation and release of mediators
What does type 1 hypersensitivity lead to
Bronchial smooth muscle contraction and bronchoconstriction
What is the late phase response
Type 4 hypersensitivity
Involves inflammatory cells, including eosinophils, mast cells, lymphocytes and neutrophils.
Cause airway inflammation
What do the eosinophils release and what does it cause
Leukotriene C4 and other mediators which are toxic to epithelial cells causing shedding of the cells
How does the inflammation affect the airways
Mucosal swelling
Thickening o bronchial walls- infiltrated by inflammatory cells
Mucus over production- dry or productive white sputum
Smooth muscle contraction
Epithelium shed and incorporated into mucus
What does long term asthma often result in
Airway remodelling
- hypertrophy and hyperplasia do smooth muscle
- hypertrophy of mucus glands
- thickening of basement membrane
Effects of airways narrowing during investigation
Wheezing
Obstructive pattern on spirometry
Air trapping with increased residual volume
-increased FRC
what type of resp failure can unmanaged mild to moderate asthma lead to
Airway narrowing leads to V/Q mismatch in affected alveoli area
Hyperventilating of better ventilated areas can’t compensate for the hypoxaemia but can for co2 retention = type 1 Resp failure
In severe cases of asthma what type of Resp failure does it show
Type 2 - blockage of airways and exhaustion limits the amount of co2 which can be breathed out
Treatment of asthma
Patient education
Drug treatment- bronchodilators and steroids
Up to date vaccinations
how can you differentiate between asthma and COPD on spirometry
Spirometry- when you give spirometers to an asthma patient their FEV will increase when you give bronchodilatprs it needs to increase by 12% in order to be asthma
what is the triad of characteristics of asthma
Triad of characteristics
- muscle constraction
- airway inflammation
- increased secretions
how does asthma present
cough wheeze breathlessness chest tightness atopy
prepipating factors for an asthma attack
allergens dust cigarette smoke cold weather exercise infections aerosols
what is difference between the coughs in COPD vs Asthma
COPD- Productive
Asthma- Dry
what pattern is seen on a spiromter in COPD and asthma
obstructive
what pattern is seen on a spiromter in COPD and asthma
obstructive
reversibility of COPD
poor- no improvement with bronchodilator
what is step 1 in asthma management - treatment
short acting beta-2-agonist
- bronchial smooth muscle relaxation
- binds to b2 receptor activates Galpha s which dissociated and binds to adenylyl cyclase converting ATP to cAMP which activates protein kinase A
Inhaled corticosteroid
-anti inflammatory
what is step 2 in asthma management
combined inhaler
-long acting beta-2-agonist- bronchial smooth muscle relaxation
-anti-inflammatory
