8. Asthma Flashcards
what type of resp. deficit is asthma
obstructive
draw the time-volume curve, and flow volume loop of a P with asthma
time-volume curve:
- FVC nearly normal
- FEV1 sig. reduced
- FEV1/FVC ratio <70%
flow-volume loop:
- PEFR reduced
- ‘scalloped’ curve
how can asthma be differentiated from COPD
Both show airway obstruction but:
- obstruction in asthma often REVERSIBLE - >15% improvement spontaneously or with bronchodilators/steroids
- obstruction in COPD NOT FULLY REVERSIBLE - <15% improvement with treatment
define the term ‘asthma’
- Chronic inflammatory disorder of the airways in susceptible Ps…
- associated with airway hyper-responsiveness to various stimuli…
- and widespread but variable airflow obstruction…
- that is often reversible, spontaneously or with treatment
describe the 2 phases of cellular response in asthma
Chronic inflammation is driven by Th2 cells:
- macrophages process and present Ag to T cells… Th2 cells preferentially activated…
- release cytokines which attract and activate inflammatory cells, inc. mast cells and eosinophils, and activate B cells which produce IgE…
Immediate response (20mins) - T1 hypersensitivity
- promotes mast cell and eosinophil degranulation… release of mediators (histamine, prostaglandin D2, leukotriene)…
- bronchial smooth muscle contraction… bronchoconstriction
Late phase response (3-12hrs later) - T4 hypersensitivity
5. eosinophils, mast cells, lymphocytes and neutrophils release mediators and cytokines… airway inflammation and epithelial cell shedding
name 5 reasons for airway narrowing during an asthma attack
- bronchial smooth muscle contraction
- mucous over-production, and abnormal mucus (thick, tenacious and slow-moving) more likely to form mucus plugs
- oedema (mucosal swelling) due to vascular leak
- thickening of bronchial walls due to infiltration by inflammatory cells
- epithelium is shed and incorporated into thick mucus
why can non-allergic stimuli like cold and exercise trigger asthma attacks
airway hyper-responsiveness: inflammatory damage can lead to exposure of sensory nerves… smooth muscle spasms
why is long term treatment with anti-inflammatory drugs important in asthma
Poor control can lead to airway remodelling, some of which may not be fully reversible, inc.
- smooth muscle hypertrophy and hyperplasia
- goblet cell hypertrophy
- basement membrane thickening
describe the clinical symptoms/signs of asthma
- recurrent, acute attacks dyspnoea
- chronic, nocturnal cough
- wheeze
- obstructive pattern on spirometry (low FEV1, FEV1/FVC, PEFR)
- use of accessory muscles of inspiration, e.g. SCM, scalene muscles
what type of resp. failure is involved in asthma and why does this occur
Mild-moderate asthma:
i) airway narrowing with reduced ventilation of affected alveoli… V/Q mismatch in affected area…
ii) hyperventilation of better ventilated areas of lung cannot compensate for hypoxia but can compensate for CO2 retention by increased CO2 exhalation
= T1RF
Severe asthma:
i) extensive airway involvement (fewer unaffected areas where hyperventilation washes out CO2) and exhaustion (limits resp. effort)… rise in CO2
= T2RF (sign of life-threatening asthma - often require assisted ventilation)
name possible asthma triggers
- allergens, eg pollen, animals
- cold air
- exercise
- air pollution, eg fumes, cigarette smoke
- drugs - NSAIDS and beta-blockers
- emotional distress
state 3 types of drug that can be used in the treatment of an acute asthma attack
nebulised bronchodilators - relievers:
- (short acting) beta-adrenoR agonists, e.g. salbutamol
- antimuscharinics, e.g. ipratropium
- oral/IV steroids - reduce inflammation
+ O2 therapy
which drugs should be used in long-term management of asthma
- inhaled corticosteroids (reduce inflammation, preventers)
- long acting beta-adrenoR agonists (bronchodilation), e.g. salmeterol - if symptom persistence, only in conjunction with steroids
why are asthma symptoms often worse at night
physiological bronchoconstriction due to PNS activation
why are beta-adrenoRs often more effective in relieving asthma than antimuscharinics
B-adrenoRs promote bronchodilation whatever the cause for bronchoconstriction, whereas antimuscharinics only effective at relieving bronchoconstriction if it is caused by PNS overstimulation
