Asthma Flashcards
How does an asthmatic lung compare to a smoker’s lung/underdeveloped lung?
Asthmatic lung & smoker’s lung/underdeveloped lung both involve chronic inflammation, which cause:
- increase in thickness of airway smooth muscle
- damaged epithelium
- thickened basement membrane
(these are what cause wheezing)
BUT smoker’s lung/underdeveloped lung also has LOSS OF ALVEOLAR SEPTA (which normally resist lung collapse)
Define asthma.
Chronic disease of airway wall and lumina characterised by airway wall inflammation and remodelling, due to an increase in airway responsiveness to a variety of stimuli, causing reversible airflow obstruction.
Name some of the cellular and chemical causes of inflammation in asthma.
- mast cells
- eosinophils
- TNF-alpha
- leukotrienes
- neutrophils (oxidative burst)
- growth factors
What are some of the different types of asthma?
Atopic (extrinsic) asthma:
- allergic asthma: airway hyper-responsiveness to a variety of stimuli
- viral induced disease
- occupational e.g. welders, farmers, bakers
Non-atopic (intrinsic) asthma: aspirin-sensitive (adults)
Aspirin acts on the arachadonic acid pathway (used to produce prostaglandins)
What stimuli can cause airway smooth muscle contraction in allergic asthma?
SPECIFIC (only affect those sensitised) Pets (dander) Histamine Dust mites (faeces) Fungal spores (damp -> mould) Aspirin
NON-SPECIFIC (can affect anybody): Respiratory tract infections Air pollutants (inc. tobacco smoke) Cold air Exercise Emotional distress/anxiety Muscarinic agonists Arachadonic acid metabolites e.g. prostaglandins, leukotrienes
note: airway hyper-responsiveness can occur in individuals who do not have asthma
What is a hypothesis which explains why allergic asthma occurs?
Hygiene hypothesis
Over-cleaning —> reduced exposure to allergens in early life —> altered immune response to allergens in later life
This also explains why allergic asthma incidence is higher in developed countries
How is asthma diagnosed clinically? What are some important questions to ask?
Recurrent symptoms of more than one of:
- polyphonic wheeze (varies in intensity/tone)
- breathlessness
- chest tightness
- dry cough (worse at night; brought on by exercise, laughter, distress)
- prolonged expiratory phase
Ask about participation in sports (avoidance of exercise as it brings on cough)
Ask about other allergic conditions/factors including: hayfever, eczema, pre-natal smoke exposure, premature birth
Ask about sleep (kept up at night by cough)
Define wheeze & stridor.
WHEEZE = abnormal high-pitched (sibilant) or low-pitched sound heard mainly during expiration due to narrowed airways
The quieter a wheeze is, the more compressed the airways are
Heard bilaterally on auscultation
STRIDOR = noise heard on breathing when the trachea/larynx is obstructed
Louder and harsher than a wheeze
What are some important signs to note in an acute asthma attack?
Use of abdominal muscles (recession)
Tracheal tug: drawing in at the base of the throat - can be felt by placing finger in the middle of the root of the neck (can also be indicative of an aneurysm in the aortic arch)
Nasal flaring
Tachypnoea
Tachycardia
Cannot complete sentences in one breath
Pulsus paradoxus = exaggerated fall in systolic BP & pulse volume during inspiration
Silent chest (minimal air movement)
Central cyanosis
All of these signs are indicative of increased expiratory effort (will soon become exhausted and asphyxiate)
What are some important examinations to perform when asthma is suspected?
CHEST:
- ?scars/deformities: sternal/pectal deformities e.g. pectus excavatum are not commonly associated with asthma, more commonly associated with chronic lung conditions such as cystic fibrosis; Harrison’s sulcus (in-drawing of costal cartilages) commonly associated with childhood asthma
- ?hyper-expansion (barrel chest): this is normal when well ??
GENERAL:
- ?eczema
- ?hayfever
- ?lethargy
- ?talk
ROOM:
- medications
- trends in chart
PERCUSSION: hyper-resonant (normal when well)
AUSCULTATION: polyphonic wheeze
?inflammation
What are some important investigations to perform when asthma is suspected?
AIRWAY FUNCTION:
- PEFR: used to monitor asthma, effort-dependent test, typically has diurnal variation (low in asthma)
- Spirometry: effort-dependent test, test reversibility of asthma by comparing results before and after giving bronchodilators (low FEV1/FVC, scalloped curve, 12%+ increase in FEV1 following salbutamol) (note: reversibility is more important diagnostically than the actual FEV1/FVC value)
- Nitrogen washout: indicates inflammation when elevated
Exercise-induced bronchoconstriction: perform spirometry before and after exercise + bronchodilator (indicates airway hyper-responsiveness)
Skin prick or [IgE]blood (detects aero-allergens, but these are mostly unavoidable anyway)
CXR: excludes other causes in chronic cases, done after severe acute exacerbations to rule out pneumothorax
Outline the management of asthma.
Education (parents & patients): recognise symptoms, how to use inhaler, when/how to access services, action plan
Prevention: weight loss, diet, stop smoking
Pharmacology:
Airway relaxants:
- beta-2 agonists (short-term & long-term) e.g. salbutamol
- muscarinic antagonists e.g. ipratropium bromide
- theophylline/aminophylline (competitive inhibitor of phosphodiesterases which break down c.AMP in smooth muscle/block adenosine receptor)
Preventers (anti-inflammatory):
- corticosteroids: reduces secretion and secretion of a no. of inflammatory cells, reduces mucus secretion by mucous glands, reduces permeability of endothelium, activates beta-2 receptors
e. g. beclomethasone - leukotriene receptor antagonists: may reduce eosinophilic inflammation (aspirin-sensitive asthma) e.g. muntelukast
What is the emergency treatment for a severe exacerbation of acute asthma?
A = Oxygen
B = continuous salbutamol & atrovent nebulisers
C = IV salbutamol (beware cardiac effects!), magnesium sulfate, aminophylline + intubate/ventilate + oral/IV steroids
Monitor PEFR & O2 saturation
What is the difference in pO2 and pCO2 in short and ongoing asthma attacks?
SHORT: (Type 1 respiratory failure)
Low pO2 = V/Q mismatch in poorly ventilated alveoli
Low pCO2 = increased respiratory rate -> more CO2 lost in non-affected parts of lungs/airways
ONGOING: (Type 2 respiratory failure)
Low pO2 = V/Q mismatch + exhaustion -> weakened respiratory effort
High pCO2 = widespread airway narrowing -> no unaffected airways/lungs which can blow off excess CO2
Therefore a normal or high pCO2 indicates life-threatening asthma
Why do asthmatic patients complain of difficulty breathing in, although the airway narrowing is worse during expiration?
Increased pressure in lungs due to airway narrowing & increased residual volume (difficulty expiring)
—> breathing close to total lung volume —> sensation of breathlessness
Less compliant lung stretching from more expanded position (hyperinflation) —> larger change in intra-thoracic pressure required to change lung volume —> sensation of difficulty breathing
What are some possible reasons why asthma is worse at night?
High vagal activity —> bronchoconstriction (+ shallower breathing)
Posture —> lung volume lower when supine
Circadian hormone secretion e.g. cortisol —> anti-inflammatory action reduced at night
