Asthma Flashcards
Definition?
Chronic respiratory condition linked to airway inflammation and hyper-responsiveness.
Risk Factors?
- Family history of atopic disease
- Male -pre-pubertal
- Female-childhood to adulthood
- Respiratory infections in infancy
- Exposure to tobacco smoke
- Premature birth and associated low birth weight
- Obesity
- Social deprivation
- Exposure to inhaled particulates
- Workplace-flour dust and isocyanates
Differentials and key signs?
- Bronchiectasis-copious sputum, frequent chest infections, a history of childhood pneumonia, and coarse lung crepitations
- COPD-Clinical features of COPD include a productive cough anddyspnoea on exertion in a person over 35 years of age whois a current or previous smoker
- Ciliary dyskinesia-clinical features include persistent moist cough present from birth.
- CF-moist coughandgastrointestinal symptoms that are often present from birth, finger clubbing, and failure to thrive in children.
- Dysfunctional breathing-breathlessness, dizziness, light-headedness, and peripheral tingling.
- Foreign body aspiration-suggested by sudden-onset cough, stridor (upper airway) or reduced chest wall movement on the affected side, bronchial breathing, and reduced or diminished breath sounds
- GORD-cough, postural and food-related symptoms, andvomiting.
- HF- orthopnoea, oedema, a history of ischaemic heart disease, and fine lung crepitations.
- Interstitial lung disease-dry cough and fine lung crepitations
- Lung cancer-persistent cough, haemoptysis, weight loss, or persistent hoarse voice.
- Pertussis-vomiting after coughing, or an inspiratory whoop
- PE-acute-onset breathlessness, pleuritic pain, haemoptysis, crackles, and sinus tachycardia.
- TB-persistent productive cough, which may be associated with breathlessness and haemoptysis
- Upper airway cough syndrome-frequent throat clearing and associated symptoms of chronic sinusitis and allergic rhinitis
- Vocal cord dysfunction-dyspnoea andstridor.
Epidemiology?
Prevalence: over 8 million
Age: children
Sex: male in childhood, reversed in adulthood
Ethnicity: N/A
Aetiology?
- Multi gene association interacting with environment (multifactorial)
- Viral, bacterial and allergens and occupational exposures can generate hypersensitivity reactions due to some pre-disposing genes.
Clinical Presentation?
- Presence of risk factors
- Recent upper resp tract infection
- Dyspnoea
- Cough
- Expiratory polyphonic wheeze
- Nasal polyposis
Pathophysiology?
• Bronchial hyperresponsiveness
• Inflammation-
• More eosinophils, thicker mucus and basement membrane and increased goblet cells and mast cells, neutrophils and t helper cells
• Smooth muscle cell hypertrophy
• Asthma-more t helper 2 cells not normally found in lungs-more humoral immunity
• Allergen binds to dendritic cell in lamina propria
• Columnar cells secrete thymic stromal lymphopoietin that conditions the dendritic cell to produce chemokines for Th2
• This stimulates IgE production via IL-13 and IL-4 to plasma cells
• Also promotes mast cells via IL-9 and eosinophils via IL-5
IgE antibodies form complexes with mast cells that detect allergens and release histamine prostaglandins and leukotrienes
• Bronchoconstriction, mucus secretion and more inflammation
first line Investigations?
resp exam
2nd line investigations?
- FeNO (confirms eosinophil inflammation- 40 ppb if no corticosteroids and 35 ppb if on),
- FEV1 /FVC ratio(<80%),
- Bronchodilator reversibility test if obstructive (demonstrate reversibility of airflow obstruction to short-acting bronchodilator, usually defined as improvement in FEV₁ by >12% and >200 mL from baseline)
- PEFR-flow rate as a comparison to patient’s personal best or normal values for height and gender
- FBC-raised neutrophils or eosinophils
- CXR-normal or hyperinflated
3rd line investigations?
- bronchial challenge test-agents stimulating hyper-responsiveness
- immunoassay for allergen-specific IgE-positive for allergen
- skin prick allergy testing-positive for allergen
Management of infrequent?
• Low dose ICS and formoterol
• Or
• Low dose ICS (beclomethasone) and SABA/salbutamol
Review after 3-6 months
Management of >twice a month first line?
- Low dose inhaled corticosteroid
- SABA
- Low dose ICS and formoterol
Management of >twice a month second line?
- Low dose ICS (beclomethasone) and SABA/salbutamol
* Leukotriene receptor antagonist (montelukast)
Management of Uncontrolled?
- High dose inhaled corticosteroid
- Short course oral corticosteroid
- SABA
- Or
- Medium dose corticosteroid and LABA (maintenance and reliever therapy-in one inhaler)
- Short course oral corticosteroid
- SABA
Ongoing first line?
- Low dose ICS and formoterol
* Management of exercise-induced bronchoconstriction
ongoing second line?
- Low dose ICS and SABA
- Management of exercise induced bronchoconstriction
- SABA
ongoing third line?
• Add leukotriene receptor antagonist
ongoing fourth line?
- Sub-lingual allergen immunotherapy for patients sensitised to house dust mite
- Theophylline
ongoing fifth line?
- Tiotropium/LAMA, then biological agents then azithromycin
* Note as steps increase, dose of ICS/oral CS does too
What two types of inhalers are there?
- Metered dose- Medicine in aerosol form and each puff is a certain dose-have to coordinate breathing and pushing down can be hard if arthritis
- Dry powder-Need to take a deep breath in -expensive
What is a spacer?
Spacers help to get all of the metered dose into the lungs without having to coordinate breaths, and increases bioavailability
Complications?
• Severe exacerbation • Moderate exacerbation • Airway remodelling • Oral candidiasis secondary to use of inhaled corticosteroids • Dysphonia-ICS • Oesophageal candidiasis-ICS • Death • Fatigue • pneumonia, • pulmonary collapse (atelectasis caused by mucus plugging of the airways), • respiratory failure, • pneumothorax, Status asthmaticus
Prognosis?
• Early airway remodelling in childhood can cause airway obstruction, but remains stable in adulthood
• Accelerated decline in lung function can cause severe exacerbations
• Need ICS for life
• Life expectancy similar to those without it
• Most episodic cases in childhood resolve
pattern of asthma during childhood tends to predictoutcome in later life
Definition-acute exacerbation?
Acute progressive worsening of symptoms in asthma, marked by decreased pulmonary function
Risk factors-E?
- Viral infection
- Uncontrolled symptoms
- High use of SABAs
- Not enough use of ICS
- Incorrect inhaler technique
- Low forced FEV1/high FeNO
- High BDR
- Smoking
- Allergen exposure/air pollution
- Atopic eczema
- Obesity/GORD
- Chronic rhinosinusitis
- Pregnancy
Differentials?
- Foreign body obstruction
- Vocal cord dysfunction
- Cardiac dysfunction
- Anaphylaxis
- Emphysema/COPD
- Carcinoid syndrome
- PE
- Allergic bronchopulmonary aspergillosis
- Pneumothorax
Epidemiology-E?
Age: N/A
Sex: Females
Ethnicity: N/A
Prevalence-300 million worldwide
Aetiology?
Exposure to irritant, allergen or infection
Sensitisation after repeated exposure triggers acute exacerbation
Clinical Presentation-E?
- Risk factors
- Cough
- Wheeze
- SOB
- Chest tightness
- Sleep disturbance
- Accessory muscle use
- Tachypnoea
- Tachycardia
- Diminished breath sounds
- Can’t speak
- Stridor
- Cyanosis
First line investigations-E?
ABCDE/resp exam, peak expiratory flow rate and oxygen sats
Second line investigations-E?
ABG and CXR
First line management-E?
- ICU admission
- Inhaled SABA
- Inhaled anti-cholinergic (ipratropium)
- Controlled oxygen-reach 93-95% then titrate off
- IV/I CS
Adjunct management -E?
• IV magnesium-bronchodilator
• Antibiotics-if evidence of infection
mechanical ventilation
Complications-E?
- Delayed response to therapy
- Pneumonia
- Pneumothorax
- Pneumomediastinum
- Resp failure
Prognosis-E?
Deaths per yr-preventable
Use of ICS decreases hospital admission and mortality rates
