Lecture 9: Obstructive airway diseases Flashcards
Give some examples of obstructive airway diseases:
- asthma
- COPD: emphysema, chronic bronchitis
What is asthma?
Chronic inflammatory airway disease
- affects small airways
- intermittent obstruction and hyper-reactivity
- usually reversible
What is the structure of the airways?
(from inside to outside)
- mucosa & pseudostratified epithelium
- submucosa
- smooth muscle
What are the 2 types of asthma?
Atopic
Non-atopic
What is atopic asthma?
-asthma
-eczema
-hayfever
Develops due to a type 1 hyerpsensitivity reaction
-first exposure to an allergen
-macrophages present this
-stimulating T helper cells
-these THcells make IgE antibodies
-IgE attach themselves to mast cells
-IgE cross over, causing mast cell degranulation
-histamines, leukotrienes, and cytokines cause inflammation (oedema), increased mucus production and bronchoconstriction causing narrowing/blockage of the small airways
What are the symptoms of asthma?
-breathless (harder to exhale)
-chest tightness
-wheeze
-cough (dry, tends to be at night, parasympathetic system: don’t take in as much oxygen, and it causes bronchoconstriction)
-atopy
(intermittent symptoms)
What are signs of asthma?
Respiratory rate: increased
Pulse: increased
Oxygen sats: low
Listening to chest: wheeze
How do we diagnose asthma with investigations?
-peak flow
-spirometry (low FEV1:FVC-obstructive)
(reversibility with bronchodilator)
How do we manage asthma?
Divide into probabilities
Low- little/no typical features (other diagnosis more likely), rule out/treat other causes
Intermediate- some symptoms/treatment for other causes aren’t working
High- typical presentation of asthma, so start treatment straight away
- patient education (remove triggers)
- pharmacology
How do we treat asthma?
Step 1:
- Promote sympathetics: bronchodilation, Beta 2 receptors in lungs, so give short acting B2 agonists
e. g. salbutamol= BLUE INHALER (RELIEVER INHALER) - BROWN INHALER (PREVENTER INHALER): corticosteroid, to reduce inflammation
Step 2: (if symptoms are bad)
- long acting beta agonist and corticosteroid: PURPLE INHALER
- still have reliever
Step 3:
- increase steroid dose
- add leukotriene receptor antagonist (this is released from mast cells)
If still no improvement, check to see if you have the correct diagnosis/ if inhaler technique is correct
How can you aid childrens asthma medication?
Add a spacer for children if they find inhaler technique hard
When do we need to give emergency management?
-(ABC) Actuely severe -can't complete full sentences -oxygen sats low >/+ 92% -resp rate increased >/=25 -wheeze -HR >/= 110 bpm -if well enough PEFR is 33-50% of best predicted value
Life-threatening
- cyanosis
- drowsy
- poor respiratory effort/silent chest-no airflow
- oxygen sats <92%
- if they can, PEFR <33%
- arrythmia/hypotension
What are the ABG’s for acute severe asthma?
Hyperventilation -low CO2 -increased pH -low pO2 as they are hypoxic =respiratory alkalosis (type 1 respiratory failure)
What are the ABG’s for life threatening asthma?
ABG’s look normal
- deteriorating
- rising pCO2, as resp rate is going down
How do we manage acute severe/life threatening asthma?
- oxygen
- salbutamol (nebuliser: mask)
- steroids (orally/IV)
- admit them
- chest X-Ray (rule out pneumothorax)
What is the difference between type 1 and 2 respiratory failure?
1: low pO2, low pCO2
2: low pO2, high pCO2
What is atopy?
Genetic tendency to develop allergic diseases
-associated with heightened immune response to common allergens
What is emphysema?
- alveolar wall damage (due to smoking)
- larger alveoli form which can’t support the smaller airways (bronchioles)
- bronchioles collapse and trap air inside the lung
Not reversible
How does alpha-1 antitrypsin deficiency effect the lungs?
genetic
Balance action of protease enzymes/elastase which are produced in presence of infection/inflammation/smoking
-if you have this disease then elastase can break down elastin in the lungs leading to destruction of alveoli and therefore emphysematous change
What is chronic bronchitis?
Chronic inflammation of the bronchioles
- not allergic
- chronic inflammation after exposure to tobacco/smoking
Irreversible
- increased mucus production
- inflammation of the airways
- less associated with bronchoconstriction (as no degranulation of mast cells) so don’t respond that well to bronchodilators
What are the clinical presentations of chronic bronchitis?
-chronic productive cough for at least 3 months consequetively
What are the risk factors for COPD?
- smoking
- more common in men
- increased age
- childhood respiratory diseases
- genetics (A1AT def)
- exposure
What are the symptoms of COPD?
Both emphysema and chronic bronchitis: breathlessness and wheeze
How doyou diagnose patients with COPD?
-Spirometry: obstructive airway pattern (reduced FEV1:FVC)
-Poor bronchodilator reversibility
-chest XRay: air trapping: dense on X-ray, and hyperinflated chest
(hyperinflated if you can see >6 anterior or >10 posterior ribs)
