Respiratory conditions Flashcards
How is asthma diagnosed?
A combination of:
- Decrease in lung function/expiratory airflow on spirometry (difficult to perform <5 years old)
AND
- Respiratory symptoms (wheeze, SOB, cough, chest tightness)
What does untreated asthma cause to the pt
- Chronic inflammation
- airway hyperresponsiveness
- Intermittent airway narrowing
Define atopic and non atopic asthma
Atopic/extrinsic
- Triggered by the environment
- Inflammation due to systemic IgA production
(smoke, animals, medications, mould etc)
Non-Atopic/intrinsic:
- Not caused by exposure to an allergen
- Inflammation due to local IgA production
(exercise, URTI, emotions, comorbid medical diseases)
Why is asthma not diagnosed <12 months?
Wheezing is usually due to bronchiolitis or small, floppy airways
Define early and late phases of asthma
Early:
- Initial allergen response within 10-20minutes
- Production of IgE-mast cell complex - release histamine and inflammatory mediators which causes smooth muscle constriction, increased cap permeability and oedema in the bronchioles.
Late phase:
- 4-8 hours after exposure
- Inflammation and airway responsiveness prolongs asthma attack
- Reaches max after a few hours-weeks
- Responsiveness to cholinergic medications as often increased
Define severe asthma
- Persistent symptoms despite treatment
- Increased risk of fatal/near fatal attacks
- Death usually due to asphyxia and associated cardiac dysrhythmias
Define uncontrolled asthma
- Poor symptom control
- Frequent exacerbations
- Serious exacerbations (ICU/hospitalization/mechanical ventilation)
- controlled asthma worsening on tapering off corticosteroids
Define a flair up/exacerbation of asthma
- Symptoms commence or become worse than usual
- Symptoms do not spontaneously resolve and require treatment
- Rapid onset or can occur over hours/days
Pathophysiology of the early stage of asthma
Dendritic cells engulf the allergen - activate - release chemokins that attract specific T-helper 2 cells.
T-helper 2 cells produce interleukins that: stimulate plasma cells to produce more IgE antibodies, binds to mast cells creating IgE-mast cell complex - releases prostiglandins, histamines and leukotrines.
This stimulates smooth muscle to bronchoconstrict, increased cap permeability, vasodilate, increase blood flow to the area.
Interleukins also stimulates bone marrow to produce eosinophils.
Pathophysiology of the late response of asthma
- Latent release of inflammatory mediators from lymphocytes, eosinophils, neutrophils
- Synthesis of leukotrines (inflammatory mediators produces by leukocytes) contributes to smooth muscle contraction
- Eosinophils cause direct injury and fibroblast proliferation
- Toxic neuropeptides increase bronchial hyperresponsiveness
- Impaired mucocilliary function (mucus trapping and removing pathogens from the airways)
- Accumulation of cellular debris forms plugs
- Increased nitric oxide causes oxidative injury and chronic inflammation
- Airway remodelling occurs (increased goblet cells and eosinophils in the tissue and mucous, thickening of basement membrane, more mast cells in the lamina propria, hypertrophy of smooth muscle cells, subepithelial fibrosis)
What does in increased airway resistance in asthma cause?
- Impaired expiration and gas trapping
- Hyperinflation distal to obstruction
- Increased WOB
- V/Q mismatch in different areas of the lungs
- hyperventilation and hypoxaemia without co2 retention - respiratory alkalosis (EARLY STAGE)
- Hyper-extension of lungs
- Thorax and respiratory muscle dysfunction
- Decreased Vt and respiratory acidosis (T2 resp failure)
- Decreased LV filling time and decreased CO due to severe hyperinflation
- Cardiorespiratory arrest
Clinical manifestations of asthma
Early:
- Chest tightness
- Expiratory wheeze
- SOB
- Dry cough
- Prolonged expiration
- Tachycardia/tachypnoea
- Increased WOB
- Wheeze during inspiration and expiration
- Pulsus paradoxus
- Hypoxaemia
Status asthmaticus:
- Not reversed by normal measures
- Effective ventilation decreases
- Respiratory acidosis
Life threatening:
- Silent chest
- PaO2 >70mmHg
Chronic asthma management
SABA (short acting beta-agonist) PRN
–>
Low dose regular preventer ICS (inhaled corticosteroid) + SABA PRN
–>
Low dose combination ICS plus LABA (long acting beta agonist) + ‘reliever’ PRN
–>
High dose ICS/LABA + ‘reliever’ PRN
Acute asthma management in adults
Mild-moderate:
4-12puffs salbutamol via MDI
Severe: 12 puffs salbutamol MDI 8 puffs ipratropium MDI (or combined in neb) O2 therapy
Life threatening:
2 x 5mg salbutamol plus ipratropium neb
O2 therapy
? ventilate
- reassess*
- give systemic corticosteroids within 1/24
Mild/moderate:
Hour of power
Severe:
Continuous nebs until symptoms resolve, then MDI
poor response?
Add IV magnesium 10mmol over 20min
Acute asthma management in paediatrics
Mild-moderate:
1- 5 years: 2-6 puffs salbutamol MDI
>6 years: 4-12puffs salbutamol via MDI
Severe:
1-5years: 6 puffs salbutamol, 4 puffs ipratropium MDI
>6years: 12 puffs salbutamol, 8 puffs ipratropium MDI
(or combined in neb 1-5 years: 2.5mg, >6years: 5mg)
O2 therapy
Life threatening:
2 x dose of salbutamol plus ipratropium neb
O2 therapy
? ventilate
- reassess*
- give systemic corticosteroids within 1/24
Mild/moderate:
Hour of power
Severe:
Continuous nebs until symptoms resolve, then MDI
poor response?
Add IV magnesium 0.1-0.2mmol/kg over 20min
What is an obstructive airway disease?
More force or time is required to exhale a volume of gas and emptying is slowed. It is associated with increased airway resistance and gas trapping.
Eg: asthma.
Clinical manifestations: Dyspnoea Decreased FEV1 V/Q mismatch Increased WOB
