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Flashcards in Asthma Deck (24)
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1
Q

What are the signs of severe asthma?

A
  • silent chest
  • cyanosis
  • tachycardia
  • bradycardia
  • hypotension
  • SpO2 < 90%
  • exhaustion/confusion
  • PaO2 <60
  • PaCO2 <36
  • acidotic
  • FEV1 <50%
  • peak expiratory flow <33%
2
Q

What are some DDx for a presentation of:

  • tachycardia
  • tachypnoea
  • hypotension
  • cyanosis
  • silent chest
  • asthma hx
A
  • 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
3
Q

How would you manage an acute asthma attack?

A

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
4
Q

What are the indications for ventilation?

What are some red flags to look for?

A

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
5
Q

What investigations would you do for an asthma exacerbation?

A

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

6
Q

List some asthma attack triggers?

A
• 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)
7
Q

Describe the pathophysiology of asthma?

A

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

8
Q

Describe the macroscopic and microscopic histopathology of asthma?

A

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)

9
Q

What might you see on an ABG following status asthmaticus?

A

• 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

10
Q

Describe the long-term management of asthma?

A

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

11
Q

List the medications available for asthma treatment?

A
  • B-adrenergic agonists (SABA and LABA)
  • Inhaled corticosteroids (ICS)
  • Muscarinic receptor antagonists
  • Xanthines
  • Leukotriene receptor antagonist
  • Sodium Cromoglycate
12
Q

What is the MA of B-adrenergic agonists? Give examples.

A

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

13
Q

Describe the dosage and SE of B-adrenergic agonists?

A

• 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)

14
Q

What is the MA of inhaled corticosteroids (ICS)? Give examples.

A

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
15
Q

Describe the dosage and SE of ICS?

A
  • 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
16
Q

What is the MA and SE profile of Muscarinic receptor antagonists? Give an example.

A

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
17
Q

What is the MA and SE profile of Xanthines? Give an example.

A

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)

18
Q

What is the MA and SE profile of Leukotriene receptor antagonists? Give an example.

A

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

19
Q

What is the MA and SE profile of Sodium Cromoglycate?

A
  • MA: inhibits mast cell release of inflammatory mediators
  • Dose: 20mg inhaled, 10 mins before exercise
  • SE: cough, throat irritation, bitter taste, transient bronchospasm
20
Q

Describe the pharm management of mild/moderate asthma?

A

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

21
Q

Describe the pharm management of severe asthma?

A

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

22
Q

Describe the pharm management of life-threatening asthma?

A

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

23
Q

How would you stabilise the asthmatic pt’s BP?

A
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)
24
Q

Describe how you would monitor this asthmatic pt long-term?

A

• 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