Obstructive Airways Disease Flashcards
ADD CARDS FROM BRIAN J LIPWORTH
ADD CARDS FROM BRIAN J LIPWORTH
What are the five steps of asthma management given by the British Thoracic Society?
- Occasional short acting inhaled B2 agonist as required for symptoms relief. If used more than once daily, or night-time symptoms, go to step 2.
- Add standard dose inhaled steroid, e.g. beclomethasone, or start at the dose most appropriate for disease severity, and titrate accordingly.
- Add long acting B2 agonist e.g. salmeterol. If benefit but still inadequate control, continue to increase dose of beclomethasone up to 800 microg/day. If no effect of LABA, stop it and review diagnosis. Leukotriene receptor antagonist or oral theophylline may be tried.
- Consider trials of: beclomethasone up to 2000 micrograms/day; modified oral release theophylline etc in conjunction with other therapy.
- Add regular oral prednisolone; continue with high dose inhaled steroids; refer to asthma clinic.
B2 Adrenoceptor agonists
What do they do? How? How fast?
Routes?
When are LABAs used?
Relax bronchial SM by increasing cAMP, act within minutes.
Best given inhilation but can also be PO or IV.
SE: tachyarrhythmias, decreased K, tremor, anxiety.
Long acting B2 agonists (e.g. salmeterol) can help nocturnal symptoms and reduce morning dips.
Corticosteroids Example What do they do? How? How fast? How to prevent oral candidiasis? Emergency
E.g. beclomethasone
The act over days to decreased bronchial mucosal inflammation.
Best inhaled to minimize systemic SE. E.g. beclomethasone via spacer but can also be PO or IV.
Rinse out mouth after use to prevent oral candidiasis.
Oral prednisolone is used in emergencies.
Emergency management of asthma
O - oxygen nebs S - salbutamol - nebs Hydrocortisone - IV; or prednisolone PO I - Ipratropium - nebs T - theophylline (aminophylliine) M - Magnesium sulphate IV CALL AN ANAESTHETIST
Amonophylline
Aka
How does it act and what does it do?
When to use it?
Metabolized to theophylline
Inhibits phosphodiesterase, this causing bronchoconstriction by increasing cAMP levels.
Used prophylactically to prevent morning dips; also useful if other adjuvant therapy is
What histopathology is seen in COPD?
CD4+ or CD8+?
The commonest finding is increased numbers of mucus secreting goblet cells in the bronchial mucosa, especially in the larger bronchi.
In contrast to asthma, the lymphocytic infiltrate is predominantly CD8+.
Squamous epithelium replaces columnar cells.
The inflammation is followed by scarring and thickening of the walls, which narrows the small airways.
What are the three main mechanisms in COPD which limit airflow in the small airways?
- Loss of elasticity and alveolar attachments of airways due to emphysema. This reduces the elastic recoil and the airways collapse during expiration.
- Inflammation and scarring cause the small airways to narrow
- Mucous secretion which blocks the airways
Each of these narrows the small airways and causes air trapping, leading to hyperinflation of the lungs, V/Q mismatch, increased work of breathing, and breathlessness
Alpha-1-Antitrypsin deficiency
What dos A-1-A do?
How does this relate to COPD?
A-1-A is an enzyme produced in the liver which diffuses to the lungs, where it inhibits proteolytic enzymes which are capable of destroying alveolar wall connective tissue.
It can contribute to the development of COPD.
Signs of COPD
Mild COPD?
Advanced COPD?
Difference in patients who are responsive to CO2 vs those who aren’t?
Mild COPD - no signs or just quiet wheezes
Advanced COPD - tachypnoea, prolonged expiration.
Chest expansion may be poor, lungs hyperinflated, and loss of usual dullness over liver and heart.
In patients who are still responsive to CO2 - usually breathless but rarely cyanosed.
In patients who are no longer responsive to CO2 - oedematous and cyanosed but rarely breathless.
Cor Pulmonale Aka What is Cor Pulmonale? Who gets it? What is it and what is it caused by? What is it characterized by?
Aka pulmonary hypertension
Defined as symptoms and signs of fluid overload secondary to lung disease.
The fluid retention and peripheral oedema is due to failure of excretion of sodium from the hypoxic kidney.
It is characterized by pulmonary hypertension and right ventricular hypertrophy.
What is the step-by-step treatment of COPD?
Give examples of each
- SABA for acute relief of symptoms e.g. salbutamol
- LABA e.g. formoterol or salmeterol
- Antimuscarinic drug - to achieve more prolonged and greater dilatation e.g. tiotropium or ipratropium
- Consider theophylline
- Combination of inhaled corticosteroid and LABA - in case patients have an unsuspected reversible element to their condition. Start with a 2 week trial of prednisolone, if there is an improvement then discontinue and start on inhaled corticosteroid.
What are the three physiological classical characteristics of asthma?
- Airflow limitation which is reversible
- Airway hyperesponsiveness to a wide range of stimuli
- Bronchial inflammation with T lymphocytes, mast cells, & eosinophils
Why does growing up in a relatively “clean” environment predispose to asthma?
This predisposes the child toward an IgE response to allergens
Why are beta blockers not given to asthmatics?
The airways have a direct parasympathetic supply, which tends to induce bronchoconstriction, and no direct sympathetic innervation.
Antagonism of the parasympathetic airway depends upon circulating adrenaline acting through B2 receptors in SM cells.
Inhibition of this effect causes bronchoconstriction and airflow limitation in asthmatic individuals.
What type of T reaction occurs in an acute asthma attack?
How does this differ in mild vs severe asthma?
Initially the inflammatory component is driven by Th2 lymphocytes which facilitate IgE synthesis.
As the disease progresses and loses its sensitivity to corticosteroids, there is greater evidence of a Th1 response.
What drugs are mast cells inhibited by?
Sodium cromoglycate and B2 agonists
What type of drug decreases the number of eosinophils?
Corticosteroids
What role do dendritic cells have in asthma?
They have a role in the initial uptake and presentation of allergens to lymphocytes.
