WK11 - Obstructive Diseases 2 Flashcards
Define Asthma
A heterogeneous disease, characterised by chronic airway inflammation.
Defined by Hx of Sx: wheeze, SOB, chest tightness and cough where Sx intensity varies over time w expiratory airflow limitations.
What are some causes of Asthma?
- conjunctivitis - blocked tear ducts
- rhinitis
- post nasal drip
Kids w asthma also associate with sinitis or rhinitis Tx
What is the prevalence of severe asthma?
High intensity Tx (cumulative total 23.5% of asthma pts)
Difficult to treat asthma = poor asthma control + high intensity Tx (17.4%)
Severe refractory asthma = poor asthma control + high intensity Tx + good adh. + correct inhaler technique (3.7%)
What are the 3 asthma phenotypes?
- Eosinophilic (50%)
- Neutrophilic (20-40%)
- Ex induced bronchospasm w/o apparent asthma (4-20% but up to 50% in elite athletes)
What is the primary patho mechanism of eosinophilic asthma?
- Type 2 helper cells cytokines (interleukins 4, 5 & 13) induce airway eoinophilia
- thickening of basement membrane
- responsive to ICS
What is the primary patho mechanism of neutrophilic asthma?
- associated w enviro irritants; often severe asthmatics
- no thickening of basement membrane
- resistant to ICS
What is the primary patho mechanism of Ex indcued bronchspasm w/o aparent asthma?
- mast cell release of prostaglandins, leukotrienes and histamines
- exacerbated by enviro irritants
- triggered by thermal and oxmotic stress of prolonged hyperventilation
What is IgE?
- antigen exposure = lymphoid tissue form antibodies
- attach to mast cells surface in bronchial wall
- re-exposure to same antigen creates antigen-antibody reaction ot surface of mast cell causing mast cell degranulation
- release chemical mediators
(histamine, eosinophils, neutrophils, chemotactic factors leukotrienes, prostaglandins, platelet activating factors)
Given as injection 2/7 - reduces inflammation and prevent hospitalisation.
What does an asthmatic airway look like?
Airway smooth muscle:
* hyperresponsiveness
* constriction
* thickening
Sup-epithelial inflammation and fibrosis
Mucus hypersecretion and impaired mucus clearance
Increased eisinophils and/or neutrophils in airway lumen
What are some risk factors of asthma?
Gender - female 2x more risk
Age - >40y
BMI - >30
What is FENO testing?
Fractional Exhaled Nitric Oxide
* quick, non-invasive testing - meausres inflammation (irriation/swelling) in airways
* measures how much nitric oxide (parts/billion) is in exhaled air
Does NOT directly test for asthma but can support diagnosis or review if current health plan is working >5y+
How to use a stethoscope to support asthma diagnosis?
Listen to lungs - hear wheeze coming from voice body in upp/low chest.
* can be in heard vocal cord dysfunction
If they wheeze too mcuh - may cause dystonia - unable to speak because of inflammation and vocal cord dysfunction.
What are some asthma triggers?
- anger, stress
- pets
- Ex
- pollen/bugs in home
- chemical fumes
- cold air
- fungus spores
- dust
- smoke
- strong odors
- pollution
What are some EIB considerations?
- can occur during Ex but can be up to 4-6hrs post Ex
- 2 hypothesis of H2O loss - thermal or osmotic
Water loss = airway cooling and dehydration.
Airway injury - role of EIB development and bronchial hyper responsiveness in athletes > healthy. - small airways = increased dehydration risk in epithelium
Chronic astmatics - airway smooth muscles exposed to plasma-derived products = contractile muscle properties change = more sensitive/hyper-responsive
Prevention is better than a cure. T or F?
TRUE
* short-term basis use of inhaled B2 agonist (SABA or SMART Rx methods)
Long-term - nil Rx to decrease EIB risk.
* ICS and leukotrienes antagonists and 5-lipoxygenease inhibitors - most used –> montelukast
Breathing technique ensure inspried air matches body temp.
Enviro - determine if pt becomes refractory to repeated Ex
Non-pharmacological approaches: masks/scarves in cold, improve CV fitness, training time
Mechanism pathway of EIB.
- Ex
- respiratory water loss
- mucosal dehydration
- increase osmolarity of airway surface liquid
- epithelium + submucosa + presence of increased cellular inflammation
- mediator release from cellular inflammation
- bronchial smooth muscle sensitivity
- bronchical smooth muscle contraction/airway narrowing
What physio. changes are seen with Ex in asthmatic pts?
- > 2/7 bouts of MIPA 8-12wks
- increase lung function
- increase asthma control * no change in airway inflammation and SABA use
What did studies on RCT mod vs vig find?
Participants have neutrophilic obese-asthma phenotype
1 bout of 45mins MI vs 30mins VI
- reduced eosinophilic airwya inflammation