Asthma Flashcards
What are the signs of severe asthma?
- silent chest
- cyanosis
- tachycardia
- bradycardia
- hypotension
- SpO2 < 90%
- exhaustion/confusion
- PaO2 <60
- PaCO2 <36
- acidotic
- FEV1 <50%
- peak expiratory flow <33%
What are some DDx for a presentation of:
- tachycardia
- tachypnoea
- hypotension
- cyanosis
- silent chest
- asthma hx
- Airway- foreign body obstruction, URTI, asthma, anaphylaxis, nasopharyngeal/bronchial carcinoma
- Alveoli- pneumonia, pulmonary oedema, COPD exacerbation
- Supporting structures of lung- pneumothorax, pleural effusion, PE
- Cardiac- MI, pericardiac effusion
How would you manage an acute asthma attack?
Primary survey to ensure patient stable (ABCDE):
A: airway- obstruction, patency (jaw thrust, chin tilt)
B: breathing
- Oxygen: 15L O2 non-rebreather mask, aim SpO2>95%
- Bronchodilation: salbutamol (100microg) and spacer, OR nebulised w O2, AND ipratropium bromide nebulised w O2
- Corticosteroids: oral prednisolone (25mg QID, x5 days), OR Budesonide inhaled
C: circulation- vitals (HR, BP, RR)
- IV normal saline (20ml/kg bolus)
- IV magnesium sulfate
- Adrenaline (if still no response, or arrest)
D: disability- GCS, BSL
E: exposure- temp, exposure and examine for injuries
- Ix: ABG (acidosis, resp failure), CXR (exclude pneumothorax)
- Escalation with Ipratripium, magneisum sulfate IV, sulbutamil, aminophylline, ventilation
- Monitoring
What are the indications for ventilation?
What are some red flags to look for?
Indications:
1) inadequate oxygenation
2) inadequate ventilation
3) inability to protect airway (GCS <8)
Red flags: • RR > 25 • SpO2 <90% • PaO2 <50 mmHg • PaCO2 >50 mmHg
What investigations would you do for an asthma exacerbation?
Initial:
• Peek expiratory flow rate (PEFR)- max speed of expiration indicating airway patency and respiratory effort ability
- 80-100% normal, <80% yellow zone, <50% red zone
• Spirometry- FEV1/FVC ratio <0.7 indicating obstructive pattern
• Pre and post bronchodilator spirometry -> 12% FEV1 increase if reversible
• CXR- exclude pneumothroax, COPD, pulmonary oedema
• ABG- respiratory acidosis, respiratory failure 2 (hypoxic, hypercapnic)
Lab:
• FBC: infection, esosinophilia (asthma)
• IgE- atopy
• Serum mast cell tryptase- anaphylaxis (released from activated mast cells)
When stable:
• Bronchical challenge test: methacholine -> hyper-responsive
• Radioallergosorben test -> allergen positive
List some asthma attack triggers?
• Inhaled allergens (e.g. dust, pollen) • Cold • Exercise • Smoking • Stress • URTI • Drugs- B-blockers, NSAIDs (COX1 blockage -> AA metabolised by 5-lipoxygenase -> leukotriene overproduction -> asthma exacerbation)
Describe the pathophysiology of asthma?
1) Airway remodelling
o Goblet cell metaplasia and hyperplasia
o Collagen subepithelial accumulation
o Smooth muscle hypertrophy and hyperplasia
o Increased vascularity
2) Airway inflammation
o Eosinophil recruitment
o Mast cell accumulation and degranulation
o Accumulation of activated T cells and macrophages
o Neutrphil recruitment
3) Functional abnormality
o Bronchoconstriction
o Airway wall oedema
o Mucus plugging
o Airway hyper-responsiveness to bronchoconstrictor or non-specific irritant
Describe the macroscopic and microscopic histopathology of asthma?
Macro:
o Hyperinflated lungs
o Atelectasis
o Mucus plugging of bronchi
Micro:
o Thickened basement membrane of bronchial epithelium
o Oedema and inflammatory cell infiltrate (eosinophils, mast cells)
o Increased size and number of submucus glands
o Goblet cell hyperplasia
o Bronchial smooth muscle hypertrophy
o Curshmann spirals- whorls of shed epithelium in mucus plugs
o Charcot Leyden crystals- crystalloid collections of eosinophil membrane protein
o Blood vessel congestion (acute)
What might you see on an ABG following status asthmaticus?
• Type 2 respiratory failure – hypoxaemia and hypercapnia
o Inadequate alveolar ventilation
o Acute: hyperventilation (increased resp drive) -> decreased PaCO2
o Chronic: mucus plugging, bronchoconstriction, airway resistance -> alveolar hypoventilation -> CO2 retention and poor oxygenation -> type 2 resp failure
• Uncompensated respiratory acidosis
- compensated: kidneys reabsorb bicarb ions in attempt to neutralise acid produced by CO2 retention -> bicarb increase AND increased H+ secretion
Describe the long-term management of asthma?
Mild asthma:
o SABA reliever
o If not controlled, add low-dose inhaled corticosteroid (ICS) preventer
Poorly controlled asthma (already taking ICS)
o Increase ICS dose
o OR continue low dose ICS and add LABA
o OR ICS-LABA combination
Severe asthma:
o Medium/high dose ICS and LABA
o OR high dose ICS-LABA combination
List the medications available for asthma treatment?
- B-adrenergic agonists (SABA and LABA)
- Inhaled corticosteroids (ICS)
- Muscarinic receptor antagonists
- Xanthines
- Leukotriene receptor antagonist
- Sodium Cromoglycate
What is the MA of B-adrenergic agonists? Give examples.
E.g.
o Short-acting (SABA, 4-6hrs)- Salbutamol, Terbutaline
o Long-acting (LABA, 12 hrs)- Salmetrol
MA: direct activation of B2 adrenergic receptors -> dilates bronchial smooth muscle
- Also inhibits inflammatory mediators of mast cells
Describe the dosage and SE of B-adrenergic agonists?
• Dose:
o SABA 200microg (2 puffs) PRN- effect in 5 mins, lasts 3-6hrs
o LABA 50microg BD, effect in 20 mins, lasts 12 hrs
• SE: CNS (tachycardia, AF, SVT), CNS (tremor, insomnia), metabolic (muscle cramps, hypokalaemia/intracellular shift, hypoglycaemia), tolerance (in overuse)
What is the MA of inhaled corticosteroids (ICS)? Give examples.
E.g. Budesonide (Pulmicort), Fluticasone (Flixotide)
• MA: glucocorticoids regulate gene transcription
- > reduced neutrophil, reduced T cell function, reduced COX2 pathway
- > reduced airway inflammation and bronchial hyper-responsiveness
Describe the dosage and SE of ICS?
- Dose: 500microg (2 puffs) BD, step down after 3/12
- SE: suppressed immunity (oral thrush), bruising, dermal thinning, adrenal suppression, altered bone metabolism (osteoporosis), impaired wound healing, diabetes, PUD, Cushing’s syndrome, dysphonia
