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
What is the MA and SE profile of Muscarinic receptor antagonists? Give an example.
E.g. Ipatropium Bromide (Atrovent)
- MA: antagonises bronchial constriction (caused by parasympathetic stimulation of M1 and M3 receptors when binding ACh)
- Dose: 21 microg, slow osnet (30-60mins) so use with SABA
- SE: tachycardia, N/V, dry mouth, blurred vision
What is the MA and SE profile of Xanthines? Give an example.
E.g. Theophylline (Neulin)
• Indication: when >2 agonists ineffective
• MA: inhibition of phosphodiesterase -> reduced intracellular c-AMP hydrolysis -> bronchodilation and pulmonary vasodilation
- Also, possibly inhibits inflam cell activation
• Dose: 300mg PO BD
• SE: CNS stimulation, cardiac stimulation, N/V, anorexia, diuresis (increased GFR)
What is the MA and SE profile of Leukotriene receptor antagonists? Give an example.
E.g. Montelukast
• MA: competitively antagonises cysteinyl leukotriene receptor (CystLT1) and blocks action of LTD4 and secondary ligands LTC4 and LTE4
-> reduced bronchial smooth m contraction from leukotrienes
• Indication: exercise-induced asthma
• Dose: 100mg PO daily, 1 hr before exercise
• SE: GIT (abdo pain, diarrhoea, N/V, LFT derangement), CNS (headache, fatigue, muscle cramps), rashes, fever
What is the MA and SE profile of Sodium Cromoglycate?
- MA: inhibits mast cell release of inflammatory mediators
- Dose: 20mg inhaled, 10 mins before exercise
- SE: cough, throat irritation, bitter taste, transient bronchospasm
Describe the pharm management of mild/moderate asthma?
Mild/moderate- can speak sentences, walk
o Salbutamol w spacer (4-12 puffs)
o Oral prednisone (within 1st hr, x5 days)
o Ipratropium bromide (8 puffs) if unresponsive
Describe the pharm management of severe asthma?
Severe- unable to speak, increased WOB, SpO2 90-94%
o Notify senior staff
o Salbutamol nebulised w air/O2
o Oral prednisone (hydrocortisone IV if PO not possible)
o Ipratropium bromide nebulised if unresponsive
Describe the pharm management of life-threatening asthma?
Life-threatening- drowsy, collapsed, exhausted, cyanotic, SpO2 <90%
o Notify senior staff
o Salbutamol nuebilised w O2 (2 x 5mg), continuous nebulisation until improves
o Hydrocortisone IV
o Ipratropium bromide nebulised if unresponsive
o Intubate if persisting
How would you stabilise the asthmatic pt’s BP?
Non-pharmacological: o Postural: elevate legs o Normal saline IV bolus (20ml/kg over 10 mins) Pharmacological: o Salbutamol (B agonist) o Adrenaline (if anaphylaxis)
Describe how you would monitor this asthmatic pt long-term?
• History
o Frequency of reliever use
o Response to current Rx
o Correct technique
o Risk factors: smoking, allergens, irritants
• Exam: vitals, respiratory distress signs
• Ix: PEFR, spirometry (3-6 months after commencing, then annually)
• Asthma action plan: symptom recognition, reliever, preventer
• Regular review of medication, compliance, symptom control
