Asthma

Question 1

def

Answer 1

chronic inflammatory airway disease characterized by variable reversible airway obstruction, airway hyper-responsiveness & bronchial inflammation

Question 2

aetiology

Answer 2

combination of genetic & environmental factors
genetic
-positive family history
-majority of asthmatics show atopy (tendency of T lymphocytes (TH2) cells to drive production of IgE on allergen exposure)
environmental
-house dust mite
-pollen
-pets
-cigarette smoke
-A. fumigates

Question 3

pathogenesis

Answer 3

EARLY PHASE (UP TO 1H)

• allergen exposure in presensitized individual causes IgE crosslinking on mast cell surface
• release of histamine, prostaglandin D2, leukotrienes, TNF-a
• induce SM contraction, mucous hypersecretion, oedema, airway obstruction

LATER PHASE (6-12H)

• recruitment of eosinophils, basophils, neutrophils, Th2 lymphocytes & their products which prolong inflammation & bronchial hyper-responsiveness
• structural cells (bronchial epithelial cells, fibroblasts, SM cells) release cytokines, profibrogenic & proliferative GFs
• contribute to inflammation & altered function & proliferation of SM cells & fibroblasts (airway remodelling)

Question 4

epi

Answer 4

10% of children
5% of adults
affects males & females equally
prevalence is increasing

Question 5

history

Answer 5

wheeze, breathlessness, cough which is worse in morning & at night

may have history of allergic rhinitis, urticaria, eczema or family history of asthma

Question 6

what precipitating factors could result in an exacerbation of asthma or an asthma attack

Answer 6

cold
viral infection
drugs (b-blockers NSAIDs)
exercise
emotions

Question 7

examination

Answer 7

tachypnoea
use of accessory muscles
prolonged expiration
polyphonic wheeze
hyperinflated chest

Question 8

examination of severe attack

Answer 8

PEFR <50% predicted
HR >110
RR >25
inability to complete sentences

Question 9

examination of life-threatening attack

Answer 9

PEFR <33% predicted
silent chest
cyanosis
bradycardia
hypotension
confusion
coma

Question 10

investigations

Answer 10

ACUTE

• peak flow
• pulse oximetry
• ABG
• CXR (to exclude other diagnoses)
• FBC (increased WCC indicates an infective exacerbation)

CHRONIC

• PEFR monitoring with diurnal variation
• pulmonary function tests show obstructive defect which improves with B2-agonist
• blood may show eosinophilia or raised IgE
• skin prick test to identify allergens

Question 11

management of an acute asthma attack

Answer 11

• resuscitate, monitor O2 sats, ABG, PEFR
• high flow O2
• nebulised B2-agonist bronchodilator salbutamol (5mg initially continuously, then 2-4hourly), ipratropium (0.5mg qds)
• steroids (100-200mg IV hydrocortisone, then 40mg oral prednisolone for 5-7days)
• if no improvement, IV magnesium sulphate
• anaesthetic help if patient becoming exhaused (rising pCO2)
• treat underlying cause (infection, pneumothorax)
• ventilation in severe attacks

Question 12

when can an asthmatic be discharged

Answer 12

• PEF >75% predicted/patient’s best
• diurnal variation <25%
• check inhaler technique
• stable for 24h
• patient owns PEF meter, has steroid & bronchodilator therapy

Question 13

management - chronic ‘stepwise’ therapy

Answer 13

1 inhaled SA B2-agonist as needed, if used >1/day move to step two
2 as above plus regular inhaled low dose steroids (400mcg/day)
3 as above plus inhaled LA B2-agonist, however if inadequate control increased steroid dose (800mcg/day), if not response to LABA stop it but increase steroid dose
4 increased inhaled steroid dose (2000mcg/day) plus fourth drug (leukotriene receptor antagonist, B2 agonist tablet)
5 additional regular oral steroids, maintain high dose inhaled steroid, however consider other treatments to minimize oral steroid use

Question 14

complications

Answer 14

growth retardation
chest wall deformity
recurrent infections
pneumothorax
respiratory failure
death

Question 15

prognosis

Answer 15

children often improve

adult-onset asthma is usually chronic