Asthma Flashcards
Definition
Chronic inflammatory condition of the lung airways
3 characteristics of asthma
Airflow limitation
Airway hyperreponsiveness
Inflammation of the bronchi
Is airflow limitation reversible?
yes, usually spontaneously/with treatment
What cell types are involved in inflammation of the bronchi?
T lymphocytes Mast cells Eosinophils Oedema SM hypertrophy Matrix deposition Mucus plugging epithelial damage
What is extrinsic asthma
Atopic - implying a definite external cause
What is intrinsic asthma
when no causative agent can be identified - often ‘late onset’
Atopy
tendency to develop IgE antibody mediated reactions against environmental antigens
genetic and environmental factors affect serum IgE levels
What are bronchial provocation tests?
Patients inhale gradually increasing concentrations of either histamine or methacholine.
Patients with clinical Sx of asthma respond to very low doses
What is the eosinophilic asthma phenotype?
allergic, Th2
- early onset, atopy associated
- later onset, non-atopic
Which cells are jam packed with granules and have high affinity IgE receptors?
mast cells
What’s mast cell sensitisation?
when mast cells get IgE associated with its IgE receptors, and its then primed to be activated
What happens when a mast cell is activated?
it releases mediators and degranulates
3 mast cell mediators and what time frame are they released in?
Histamine seconds
Eicosanoids minutes
Cytokines hours
what is a very potent bronchoconstrictor?
histamine
What are cys-LT1 and cys-LT2?
cysteinyl-leukostrienes (a type of eicosanoid)
Precipitating factors for asthma
major allergens viral infections cold air exercise irritant dusts vapours and fumes emotion & drugs
Pathophysiology: what happens to the SM, epithelial cells and the basement membrane?
SM - inappropriate + excessive contraction of SM. hypertrophy + proliferation of SMCs
Epithelial cells - may be abnormal, altered expression of matrix regulating proteins. neoplasia: increase in number of goblet cells
BM - increased thickening
What makes the airway narrow?
SM contraction
thickening of the airway by cellular infiltration
secretions within the airway lumen
Presentation
cough + chest tightness
diurnal variation
worse at nights and early morning
provoked by triggers
Presentation during an attack
reduced chest expansion, prolonged expiratory time and bilateral polyphonic wheezing
Diagnostic tests
Skin prick test
CXR- hyperinflation?
PaO2 and PaCO2 down –> hyperventilation
Variable airflow limitation
Diurnal variation of PEFR - increased after inhalation of bronchodilator (reversibility testing)
How would you rule out bronchopulmonary aspergillosis ?
CXR
which out of bronchodilators and steroids alleviate symptoms and which target inflammation?
BDs- alleviate Sx
steroids- target inflammation
What’s step 1 for BTS stepwise treatment for asthma?
occasional SABA for symptom relief e.g. salbutamol
short acting beta-2 agonist
if SABA isn’t sufficient, what Tx would you add?
standard-dose inhaled steroid e.g. beclometasone
when would you add salmeterol to Tx and review Dx?
its a LABA.
would add to inhaled steroid and SABA
(step 3)
What’s step 4 for BTS stepwise treatment for asthma?
consider trials of high beclometasone (inhaled steroid)
If all else fails, whats the final step in Tx?
regular oral prednisolone
What’s the molecular difference between SABAs and LABAs?
a LABA is a SABA with an added long lopophilic chain
how to B2-adrenoceptor agonists work?r
they relax bronchial smooth muscles (increasing cAMP), acting within minutes
Mx for a really severe asthma attack?
02 40-60%, salbutamol nebuliser, prednisolone
