Asthma Flashcards
What is the definition of asthma?
Chronic inflammatory disorder of airways characterised by bronchial hyperactivity to stimuli which leads to airways obstruction (can be irreversible)
What changes occur in the bronchioles in someone with asthma?
SM contraction
SM hypertrophy= thickening of walls
BM membrane thickening
Mucous and exudate in lumen
What are the 3 main causes of airway obstruction in asthma?
Inflammatory cell infiltration by TH cells, lymphocytes, eosinophils and mast cells
Mucus hypersecretion and mucus plug formation
SM contraction
What changes occur microscopically in asthma?
Desquamated epithelial cells
Eosinophil membranes
Infiltration of inflammatory cells i.e. CD4 lymphocytes
How is the hygiene hypothesis related to asthma?
Early life exposure to bacterial endotoxins switches off allergic response
I.e. lack of early exposure can lead to increase risk of developing asthma
What are the main factors leading to the development of asthma?
Environmental
-asthma after 12= likely environmental cause
Genetic:
- Asthma before 12= genetic link
- FH has important role in asthma
What is the trilogy of conditions referred to as atopy?
Allergic rhionitis
Asthma
Eczema
What are the 2 types of triggers for asthma? Give examples of each.
Inducers= enhance inflammatory response
- allergens
- viral infection
- occupational exposure
- animal fur
- dust
- mould
- aerosols
Provokers= activate bronchospasm
- exercise
- cold air
- stress
- aspirin
What are the classic presenting symptoms? What are the characteristics of these symptoms?
Episodic breathlessness (SOB)
Cough
Wheezing
Chest tightness
Variable and intermittent
Diurnal variation= worse at night
Associated with triggers
What are clinical signs to look out for on examination?
Wheeze= polyphonic and expiratory
Hyperinflation (associate with longstanding or poorly controlled asthma)
-pronounced pectoral and SCM muscles due to increased use of accessory muscles for breathing
No wheeze and silent chest= life-threatening asthma
How is the wheeze for asthma different from that associated with tracheal/subglottic stenosis?
Asthma
- polyphonic= due to multiple small airways being affected
- expiratory
Tracheal stenosis:
- monophonic= single tone due to narrowing of large airway
- inspiratory
What are the components required for diagnosis of asthma?
Day to day peak flow variability Asthma symptoms Airway hyperresponsiveness Reversibility of airway obstruction i.e. >15% increase in FEV1 after single dose of SABA or several weeks of steroids
How is a peak flow used to support the diagnosis of asthma?
Diurnal variation
-20% variation in PEF for >3/7 days
How can spirometry be used to support a diagnosis of asthma?
Can show an obstructive pattern i.e. decrease forced expiratory volume in 1 second (FEV1)
What are the possible differentials for asthma?
Upper airway obstruction
-can cause wheeze BUT it is monophonic
COPD
-irreversible
Tracheal tumour
GORD
-micro aspiration of acid= can cause inflammatory response in airways
Interstitial lung diease
HF
Pulmonary hypertension
Chronic thromboembolic disease
Bronchiectasis
What are the non-pharmacological managements of asthma?
Smoking cessation
Weight reduction in obesity
Allergen avoidance in sensitised individuals
How is asthma managed pharmacologically? What are the different classifications of drugs and their basic mechanism?
Step wise approach (most appropriate TX for severity) to gain early control
Selective Beta-2 agonist= RELIEVER (blue inhaler)
Eg= salbutamol + terbutaline
Mech= bronchodilation
Inhaled corticosteroids= PREVENTER (brown inhaler)
Eg= Beclometason + Fluticason + Budesonide
Mech= acts as anti-inflammatory
Long-acting beta-2 agonist= LABARs
Eg= Salmeterol + Foromoterol
Mech= used in combo with steroids on step 3 of asthma management
Leukotrienes receptor antagonist= ADD ON to inhaled steroids
Eg= Montelukast
Mech= target leukotrienes as a prophylaxis for asthma
Xantaine derivatives= ADD ON to relieve acute bronchospasm
Eg= IV aminophyline (specialist use only)
Mech= non-selective phosphodiesterase inhibitors to interfer with bronchial SM
Long acting antimuscarinics= LAMAs
Eg= Tiotropium
Mech= bronchodilators in severe asthma
What are the 3 different levels of severity of acute severe asthma?
Moderate:
- increasing symptoms
- PEFR 50-75% of predicted or best
Severe: (any one of)
- PEFR 33-50%
- RR> 25
- HR>110
- inability to complete sentence in one breath
Life threatening:
- PEFR <33%
- Sats <92%
- PaO2 <8kPA
- cyanosis
- silent chest
- bradycardia
- hypotension
- exhasution
- confused
- coma
I.e CHEST C= cyanosis H= hypotension E= exhaustion S- silent chest T- tachy/Brady/arrhythmia
Why is it important to look at changes in CO2 levels in someone with severe asthma?
Severe asthma= CO2 normally low due to hyperventilation
Rising= life-threatening attack
Normal= patient is tiring i.e. unable to breath enough
How is a patient with acute severe asthma managed?
Sit upright
High flow oxygen via non-rebreath mask
Salbutamol (5mg) + ipratropium (0.5mg) nebs
Steroids= 100mg IV hydrocortisone or 40mg PO prednisolone
Inhaled ipratropium bromide (SAMA) 500mg every 4-6 hrs via O2 driven neb
MgSO4= 2g IV
Inform ITU as may need to be intubated
Monitor ECG
-due to salbutamol increased HR
Once a patient with severe acute asthma is stabilised, what can be done to monitor them?
PEFR every 15-30 mins
SpO2 maintained above 92%
ABG (if initial CO2 normal or high)
Oral prednilosone 15mg 1x day for 5 days
Neb salbutamol every 5 hrs
What are the signs of asthma on CXR?
Hyper expansion with flattened hemi-diaphragms
What are the possible adverse effects of using a high dose nebuliser SABA?
Tremor
tachycardia due to cross reaction with B1 receptor in heart
Decreased K+ due to action on Na+/K+ ATPase causing increased uptake of K+ by cells
What are the possible adverse affects of using inhaled corticosteroids?
Oral candidiasis (oral thrush) -can be due to poor technique and lack of use of spacer
Osteoporosis
Growth suppression
What are the common reasons for poor response to asthma treatment?
Non-adherence
- poor understanding
- trouble managing polypharmacy
- stress
- complicated regiment
Poor technique
Presence of inducers
Wrong diagnosis
